Publications by authors named "Jingshan Shi"

79 Publications

Resveratrol against 6-OHDA-induced damage of PC12 cells via PI3K/Akt.

Transl Neurosci 2021 Jan 19;12(1):138-144. Epub 2021 Apr 19.

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, No. 6, Xuefu West Road, Xinpu New District, Zunyi 563000, Guizhou, China.

Objective: Our previous study found that resveratrol (Res), which is a phytoalexin, attenuated 6-hydroxydopamine (6-OHDA)-induced motor dysfunction by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway in rats. Therefore, we further explored the protective effect of Res on 6-OHDA-induced damage to PC12 cells with respect to the PI3K/Akt signaling pathway.

Methods: We incubated PC12 cells with 75 μM 6-OHDA for 24 h, and Res was then added at a final concentration of 25 μM; the protective effect was examined via MTT and lactate dehydrogenase (LDH) assays. In addition, the PI3K inhibitor LY294002 was used to investigate the potential mechanism. JC-1 staining was used to detect the mitochondrial membrane potential (MMP), and western blotting (WB) was used to detect the phosphorylation of Akt-Ser473.

Results: Compared with that in the control, the cell viability, total superoxide dismutase (SOD) activity, MMP, and p-Akt-Ser473 level of 6-OHDA-treated PC12 cells were significantly decreased, while the leakage rate of LDH was increased. And after treatment with 25 μM Res, the cell viability, total SOD activity, MMP, and p-Akt-Ser473 level of 6-OHDA-treated PC12 cells were significantly increased compared with those of the control cells, while the leakage rate of LDH was decreased. These effects of Res were antagonized by LY294002.

Conclusions: Res ameliorates 6-OHDA-induced damage to PC12 cells via activation of the PI3K/Akt signaling pathway.
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http://dx.doi.org/10.1515/tnsci-2020-0165DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8060978PMC
January 2021

Lindl. alkaloids alleviate Mn-induced neurotoxicity via PINK1/Parkin-mediated mitophagy in PC12 cells.

Biochem Biophys Rep 2021 Jul 2;26:100877. Epub 2021 Apr 2.

Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, China.

Modern pharmacological studies have demonstrated that Lindl. Alkaloids (DNLA), the main active ingredients of , is valuable as an anti-aging and neuroprotective herbal medicine. The present study was designed to determine whether DNLA confers protective function over neurotoxicant manganese (Mn)-induced cytotoxicity and the mechanism involved. Our results showed that pretreatment of PC12 cells with DNLA alleviated cell toxicity induced by Mn and improved mitochondrial respiratory capacity and oxidative status. Mn treatment increased apoptotic cell death along with a marked increase in the protein expression of Bax and a decrease in the expression of Bcl-2 protein, all of which were noticeably reversed by DNLA. Furthermore, DNLA significantly abolished the decrease in protein levels of both PINK1 and Parkin, and mitigated the increased expression of autophagy marker LC3-II and accumulation of p62 caused by Mn. These results demonstrate that DNLA inhibits Mn induced cytotoxicity, which may be mediated through modulating PINK1/Parkin-mediated autophagic flux and improving mitochondrial function.
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http://dx.doi.org/10.1016/j.bbrep.2020.100877DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8047462PMC
July 2021

Isorhynchophylline Ameliorates Cerebral Ischemia/Reperfusion Injury by Inhibiting CX3CR1-Mediated Microglial Activation and Neuroinflammation.

Front Pharmacol 2021 12;12:574793. Epub 2021 Feb 12.

Key Laboratory of Basic Pharmacology of Ministry of Education, Department of Pharmacology, Zunyi Medical University, Zunyi, China.

Reperfusion therapy is an effective way to rescue cerebral ischemic injury, but this therapy also shows the detrimental risk of devastating disorders and death due to the possible inflammatory responses involved in the pathologies. Hence, the therapy of ischemia/reperfusion (I/R) injury is a great challenge currently. Isorhynchophylline (IRN), a tetracyclic oxindole alkaloid extracted from , has previously shown neuroprotective and anti-inflammatory effects in microglial cells. This study systematically investigates the effect of IRN on I/R injury and its underlying mechanism. The effects of IRN on neuronal injury and microglia-mediated inflammatory response were assessed on a rat model with middle cerebral artery occlusion (MCAO) and reperfusion-induced injury. We found that IRN treatment attenuated the infarct volume and improved the neurological function in I/R injury rats. IRN treatment also reduced the neuronal death rate, brain water content, and aquaporin-4 expression in the ischemic penumbra of I/R injury rats' brains. Besides, IRN treatment could inhibit the following process, including IκB-α degradation, NF-κB p65 activation, and CX3CR1 expression, as well as the microglial activation and inflammatory response. These findings suggest that IRN is a promising candidate to treat the cerebral I/R injury via inhibiting microglia activation and neuroinflammation.
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http://dx.doi.org/10.3389/fphar.2021.574793DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7907603PMC
February 2021

Epigenetic Regulation of PDX-1 in Type 2 Diabetes Mellitus.

Diabetes Metab Syndr Obes 2021 2;14:431-442. Epub 2021 Feb 2.

Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, 563000, People's Republic of China.

Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by hyperglycemia which is caused by insufficient insulin secretion or insulin resistance. Interaction of genetic, epigenetic and environmental factors plays a significant role in the development of T2DM. Several environmental factors including diet and lifestyle, as well as age have been associated with an increased risk for T2DM. It has been demonstrated that these environmental factors may affect global epigenetic status, and alter the expression of susceptible genes, thereby contributing to the pathogenesis of T2DM. In recent years, a growing body of molecular and genetic studies in diabetes have been focused on the ways to restore the numbers or function of β-cells in order to reverse a range of metabolic consequences of insulin deficiency. The pancreatic duodenal homeobox 1 (PDX-1) is a transcriptional factor that is essential for the development and function of islet cells. A number of studies have shown that there is a significant increase in the level of DNA methylation of PDX-1 resulting in reduced activity in T2DM islets. The decrease in PDX-1 activity may be a critical mediator causing dysregulation of pancreatic β cells in T2DM. This article reviews the epigenetic mechanisms of PDX-1 involved in T2DM, focusing on diabetes and DNA methylation, and discusses some potential strategies for the application of PDX-1 in the treatment of diabetes.
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http://dx.doi.org/10.2147/DMSO.S291932DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7866918PMC
February 2021

RNA-Seq analysis of the protection by Dendrobium nobile alkaloids against carbon tetrachloride hepatotoxicity in mice.

Biomed Pharmacother 2021 May 6;137:111307. Epub 2021 Feb 6.

Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, China. Electronic address:

Objective: Dendrobium nobile is a genuine Chinese medicine. Dendrobium nobile Lindl. alkaloids (DNLA) protects against CCl-induced acute liver injury. This study used RNA-Seq to explore the mechanisms.

Methods: Mice were pretreated with DNLA (10 and 20 mg/kg, po) for 7 days, and subsequently intoxicated with CCl (20 μL/kg, ip for 24 h). Liver RNA was extracted and subjected to RNA-Seq. The bioinformatics, including PCA, GO, KEGG, two-dimensional clustering, Ingenuity Pathways Analysis (IPA), and Illumina BaseSpace Correlation Engine (BSCE) were used to analyze the data. qPCR was performed on selected genes to verify RNA-Seq results.

Results: DNLA protection against CCl hepatotoxicity was confirmed by histopathology. PCA revealed the distinct gene expression patterns between the different treatment groups. GO showed that CCl induced the activation, adhesion and proliferation of immune cells. KEGG showed CCl induced oxidative stress, diseases and compromised adaptive responses. CCl induced differentially expressed genes (DEGs) were identified by DESeq2 with Padj < 0.05 and 2D-clustered with other groups. DNLA reverted CCl-induced DEGs in a dose-dependent manner. qPCR analysis of S100 g, Sprr1, CCL3/7, Saa2/3, IL1rn, Cox7a2 and Rad15 confirmed RNA-Seq results. IPA showed that CCl treatment altered some signaling and metabolic pathways, which were ameliorated or returned to normal following DNLA treatment. The CCl-activated mitochondrial oxidative phosphorylation was illustrated as an example. IPA Upstream Regulator Analysis further revealed the activated or inhibited molecules and chemicals that are responsible for CCl-induced DEGs, and DNLA attenuated these changes. BSCE analysis verified that CCl-induced DEGs were highly correlated with the GEO database of CCl hepatotoxicity in rodents, and DNLA dose-dependently attenuated such correlation.

Conclusion: RNA-Seq revealed CCl-induced DEGs, disruption of canonical pathways, activation or inhibition of upstream regulators, which are highly correlated with database for CCl hepatotoxicity. All these changes were attenuated or returned to normal by DNLA, demonstrating the mechanisms for DNLA to protect against CCl hepatotoxicity.
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http://dx.doi.org/10.1016/j.biopha.2021.111307DOI Listing
May 2021

Rutaecarpine Ameliorates Pressure Overload Cardiac Hypertrophy by Suppression of Calcineurin and Angiotensin II.

Evid Based Complement Alternat Med 2021 12;2021:8857329. Epub 2021 Jan 12.

Department of Pharmacology, Chongqing Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing Medical University, Chongqing 400016, China.

Cardiac hypertrophy is a major pathological process to result in heart failure and sudden death. Rutaecarpine, a pentacyclic indolopyridoquinazolinone alkaloid extracted from with multiple pharmacological activities, yet the underlying protective effects and the mechanisms on cardiac hypertrophy remain unclear. This study aimed to evaluate the potential effects of rutaecarpine on pressure overload cardiac hypertrophy. Cardiac hypertrophy in rat was developed by abdominal aortic constriction (AAC) for 4 weeks, which was improved by rutaecarpine supplementation (20 or 40 mg/kg/day, i.g.) for another 4 weeks. The level of angiotensin II was increased; the mRNA expression and the activity of calcineurin in the left ventricular tissue were augmented following cardiac hypertrophy. Rutaecarpine administration decreased angiotensin II content and reduced calcineurin expression and activity. Noteworthily, in angiotensin II-induced cardiomyocytes, rutaecarpine ameliorated the hypertrophic effects in a dose-dependent manner and downregulated the increased mRNA expression and activity of calcineurin. In conclusion, rutaecarpine can improve cardiac hypertrophy in pressure overload rats, which may be related to the inhibition of angiotensin II-calcineurin signal pathway.
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http://dx.doi.org/10.1155/2021/8857329DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7822676PMC
January 2021

AMPK: A bridge between diabetes mellitus and Alzheimer's disease.

Behav Brain Res 2021 02 8;400:113043. Epub 2020 Dec 8.

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of the Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, China. Electronic address:

The pathogenesis and etiology of diabetes mellitus (DM) and Alzheimer's disease (AD) share many common cellular and molecular themes. Recently, a growing body of research has shown that AMP-activated protein kinase (AMPK), a biomolecule that regulates energy balance and glucose and lipid metabolism, plays key roles in DM and AD. In this review, we summarize the relevant research on the roles of AMPK in DM and AD, including its functions in gluconeogenesis and insulin resistance (IR) and its relationships with amyloid β-protein (Aβ), Tau and AMPK activators. In DM, AMPK is involved in the regulation of glucose metabolism and IR. AMPK is closely related to gluconeogenesis, which can not only be activated by the upstream kinases liver kinase B1 (LKB1), transforming growth factor β-activated kinase 1 (TAK1), and Ca/calmodulin-dependent protein kinase kinase β (CaMKKβ) but also regulate the downstream kinases glucose-6-phosphatase (G-6-Pase) and phosphoenolpyruvate carboxy kinase (PEPCK), thereby affecting gluconeogenesis and ameliorating DM. Moreover, AMPK can regulate glucose transporter 4 (GLUT4) and free fatty acids to improve IR. In AD, AMPK can ameliorate abnormal brain energy metabolism, not only by reduces Aβ deposition through β-secretase but also reduces tau hyperphosphorylation through sirtuin 1 (SIRT1) and protein phosphatase 2A (PP2A). Therefore, AMPK is a bridge between DM and AD.
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http://dx.doi.org/10.1016/j.bbr.2020.113043DOI Listing
February 2021

Changes in global Orchidaceae disease geographical research trends: recent incidences, distributions, treatment, and challenges.

Bioengineered 2021 Dec;12(1):13-29

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University , Zunyi, Guizhou, China.

Many of the Orchidaceae species are threatened due to environmental changes and over exploitation for full fill global demands. The main objective of this article was critically analyzed the recent global distribution of Orchidaceae diversity, its disease patterns, microbial disease identification, detection, along with prevention and challenges. Critical analysis findings revealed that Orchidaceae growth and developments were affected indirectly or directly as a result of complex microbial ecological interactions. Studies have identified many species associated with orchids, some are pathogenic and cause symptoms such as soft rot, brown rot, brown spot, black rot, wilt, foliar, root rot, anthracnose, leaf spot. The review was provided the comprehensive data to evaluate the identification and detection of microbial disease, which is the most important challenge for sustainable cultivation of Orchidaceae diversity. Furthermore, this article is the foremost of disease triggering microbes, orchid relations, and assimilates various consequences that both promoted the considerate and facts of such disease multipart, and will permit the development of best operative disease management practices.
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http://dx.doi.org/10.1080/21655979.2020.1853447DOI Listing
December 2021

Signaling mechanisms underlying inhibition of neuroinflammation by resveratrol in neurodegenerative diseases.

J Nutr Biochem 2021 02 18;88:108552. Epub 2020 Nov 18.

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Guizhou, China. Electronic address:

Neurodegenerative diseases (NDs), including Alzheimer's disease (AD), and Parkinson's disease (PD), are characterized by the progressive loss of the structure and function of neurons and most commonly occur in the elderly population. Microglia are resident macrophages of the central nervous system (CNS). The neuroinflammation caused by excessive microglial activation is closely related to the onset and progression of many NDs. Therefore, inhibiting excessive microglial activation is a potential drug target for controlling neuroinflammation. In recent years, natural products as modulators of microglial polarization have attracted considerable attention in the field of NDs therapy. Furthermore, resveratrol (RES) has been found to have a protective effect in NDs through the inhibition of microglial activation and the regulation of neuroinflammation. In this review, we mainly summarize the therapeutic potential of RES and its various molecular mechanisms in the treatment of NDs through the modulation of microglial activation.
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http://dx.doi.org/10.1016/j.jnutbio.2020.108552DOI Listing
February 2021

Corrigendum: Combination Treatment of Icariin and L-DOPA Against 6-OHDA-Lesioned Dopamine Neurotoxicity.

Front Mol Neurosci 2020 29;13:605722. Epub 2020 Oct 29.

Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, China.

[This corrects the article DOI: 10.3389/fnmol.2018.00155.].
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http://dx.doi.org/10.3389/fnmol.2020.605722DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7658550PMC
October 2020

The use of DNA methylation clock in aging research.

Exp Biol Med (Maywood) 2021 Feb 11;246(4):436-446. Epub 2020 Nov 11.

Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, 66367Zunyi Medical University, Zunyi 563003, China.

One of the key characteristics of aging is a progressive loss of physiological integrity, which weakens bodily functions and increases the risk of death. A robust biomarker is important for the assessment of biological age, the rate of aging, and a person's health status. DNA methylation clocks, novel biomarkers of aging, are composed of a group of cytosine-phosphate-guanine dinucleotides, the DNA methylation status of which can be used to accurately measure subjective age. These clocks are considered accurate biomarkers of chronological age for humans and other vertebrates. Numerous studies have demonstrated these clocks to quantify the rate of biological aging and the effects of longevity and anti-aging interventions. In this review, we describe the purpose and use of DNA methylation clocks in aging research.
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http://dx.doi.org/10.1177/1535370220968802DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7885055PMC
February 2021

Regulation of SIRT3 on mitochondrial functions and oxidative stress in Parkinson's disease.

Biomed Pharmacother 2020 Dec 28;132:110928. Epub 2020 Oct 28.

Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563003, China. Electronic address:

Sirtuin-3 (SIRT3) is a NAD-dependent protein deacetylase that is located in mitochondria, regulating mitochondrial proteins and maintaining cellular antioxidant status. Increasing evidence demonstrates that SIRT3 plays a role in degenerative disorders including Parkinson's disease (PD), which is a devastating nervous system disease currently with no effective treatments available. Although the etiology of PD is still largely ambiguous, substantial evidence indicates that mitochondrial dysfunction and oxidative stress play major roles in the pathogenesis of PD. The imbalance of reactive oxygen species (ROS) production and detoxification leads to oxidative stress that can accelerate the progression of PD. By causing conformational changes in the deacetylated proteins SIRT3 modulates the activities and biological functions of a variety of proteins involved in mitochondrial antioxidant defense and various mitochondrial functions. Increasingly more studies have suggested that upregulation of SIRT3 confers beneficial effect on neuroprotection in various PD models. This review discusses the mechanism by which SIRT3 regulates intracellular oxidative status and mitochondrial function with an emphasis in discussing in detail the regulation of SIRT3 on each component of the five complexes of the mitochondrial respiratory chain and mitochondrial antioxidant defense, as well as the pharmacological regulation of SIRT3 in light of therapeutic strategies for PD.
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http://dx.doi.org/10.1016/j.biopha.2020.110928DOI Listing
December 2020

Abnormal Homocysteine Metabolism: An Insight of Alzheimer's Disease from DNA Methylation.

Behav Neurol 2020 8;2020:8438602. Epub 2020 Sep 8.

Department of Pharmacology and the Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi 563000, China.

Alzheimer's disease (AD) is a chronic neurodegenerative disease in the central nervous system that has complex pathogenesis in the elderly. The current review focuses on the epigenetic mechanisms of AD, according to the latest findings. One of the best-characterized chromatin modifications in epigenetic mechanisms is DNA methylation. Highly replicable data shows that AD occurrence is often accompanied by methylation level changes of the AD-related gene. Homocysteine (Hcy) is not only an intermediate product of one-carbon metabolism but also an important independent risk factor of AD; it can affect the cognitive function of the brain by changing the one-carbon metabolism and interfering with the DNA methylation process, resulting in cerebrovascular disease. In general, Hcy may be an environmental factor that affects AD via the DNA methylation pathway with a series of changes in AD-related substance. This review will concentrate on the relation between DNA methylation and Hcy and try to figure out their rule in the pathophysiology of AD.
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http://dx.doi.org/10.1155/2020/8438602DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7495165PMC
September 2020

Osthole Improves Cognitive Function of Vascular Dementia Rats: Reducing Aβ Deposition via Inhibition NLRP3 Inflammasome.

Biol Pharm Bull 2020 ;43(9):1315-1323

Department of Pharmacology, Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University.

Vascular dementia (VD) is a common neurodegenerative disease, and the cognitive dysfunction is a major manifestation of VD. Lots of evidences showed that beta-amyloid (Aβ) deposition and neuroinflammation act as vital elements in the progress of VD. The previous studies showed that osthole (OST) can improve the cognitive function of VD and Alzheimer's disease (AD). However, the effect of OST on Aβ in VD brain is still unclear. Chronic cerebral hypoperfusion (CCH) of rats were used to investigate the effect of OST on Aβ through nod-like receptor protein 3 (NLRP3) inflammasome in this study. Morris Water Maze and Y-maze were used to test the spatial learning, memory and working abilities. Hematoxylin-eosin (H&E) and Nissl staining were used to observe the morphology and number of hippocampal neurons. Immunofluorescence staining was used to observe the number of microglia activated. Western blot was used to detect the expression of proteins. The study results showed that OST obviously enhanced the spatial learning, memory and working abilities induced by modified bilateral common carotid artery occlusion (BCCAO) in rats, improved the pathological damage of hippocampal neurons induced by BCCAO in rats, inhibited the activation of microglia induced by BCCAO in rats. Furthermore, this study also discovered that OST reduced Aβ deposition in VD hippocampus via inhibition the NLRP3 inflammasome. Together, these results suggest that OST reduces Aβ deposition via inhibition NLRP3 inflammasome in microglial in VD.
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http://dx.doi.org/10.1248/bpb.b20-00112DOI Listing
January 2020

Dendrobium nobile Lindl. alkaloids-mediated protection against CClinduced liver mitochondrial oxidative damage is dependent on the activation of Nrf2 signaling pathway.

Biomed Pharmacother 2020 Sep 11;129:110351. Epub 2020 Jun 11.

Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China. Electronic address:

The activation of nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated signaling pathway has been involved in the mechanisms of a variety of protective agents against cellular oxidative stress. We recently demonstrated that Dendrobium nobile Lindl. alkaloids (DNLA), the active ingredients of Dendrobium, protects mice from CCl-induced liver injury, dependent on the Nrf2 signaling pathway. The present study was aimed to determine whether the protection against mitochondrial oxidative damage plays a role in the mode of action of DNLA on CCl-induced liver injury, and to further investigate whether the DNLA-conferred mitochondrial beneficial effects is dependent on the activation of Nrf2 signaling. The CCl-induced acute liver injury model was employed in both wild-type (WT) and Nrf2-knockout (Nrf2) mice. The results showed that in WT mice DNLA reduced CCl-induced liver injury, accompanied by a significant reduction in CCl-induced mitochondrial oxidative stress as evidenced by a decrease in mitochondrial HO content and MDA production, and a marked increase in GSH level and Mn-SOD activity. However, these protective effects were significantly attenuated in Nrf2 mice. Furthermore, the administration of DNLA improved mitochondrial oxygen consumption, elevated ATP production, and decreased CCl-induced apoptosis in the WT mice, whereas the DNLA-mediated protections on mitochondrial function were diminished in the Nrf2 null mice. These results demonstrate that the improvement of mitochondrial oxidative stress and mitochondrial dysfunction is implicated in the mechanism of DNLA-mediated protection on CCl-induced liver injury, and this DNLA-modulated mode of action is dependent on the activation of Nrf2 signaling pathway.
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http://dx.doi.org/10.1016/j.biopha.2020.110351DOI Listing
September 2020

Icariside II, a PDE5 Inhibitor, Suppresses Oxygen-Glucose Deprivation/Reperfusion-Induced Primary Hippocampal Neuronal Death Through Activating the PKG/CREB/BDNF/TrkB Signaling Pathway.

Front Pharmacol 2020 24;11:523. Epub 2020 Apr 24.

Department of Clinical Pharmacotherapeutics, School of Pharmacy, Zunyi Medical University, Zunyi, China.

Background: Ischemic stroke remains the leading cause of death and adult disability. Cerebral ischemic/reperfusion (I/R) injury is caused by ischemic stroke thereafter aggravates overwhelming neuronal apoptosis and even the death of neurons. Of note, hippocampus is more susceptive to cerebral I/R injury than the other brain region. This study was designed to explore the effects and mechanism of icariside II (ICS II), a pharmacologically active compound exists in herbal with previous study-proved as a phosphodiesterase 5 (PDE5) inhibitor, on the oxygen glucose deprivation/reoxygenation (OGD/R)-induced primary hippocampal neurons injury.

Methods: Effects of ICS II on primary hippocampal neuronal impairment and apoptosis induced by OGD/R were examined by MTT, lactate dehydrogenase (LDH) release, TUNEL staining, and flow cytometry, respectively. Activation of memory-related signaling pathways was measured using Western blot analysis. The direct interaction between ICS II and PDE5 was further evaluated by molecular docking.

Results: ICS II (12.5, 25, 50 μM) markedly abrogated OGD/R-induced hippocampal neuronal death as suggested by the increase in neurons viability and the decrease in cellular LDH release. Furthermore, ICS II not only effectively decreased the protein expression and activity of PDE5, restored the 3'5'-cyclic guanosine monophosphate (cGMP) level and its downstream target protein kinase G (PKG) activity but also increased the phosphorylation of cAMP response element binding protein (CREB) level, expressions of brain derived neurotrophic factor (BDNF), and tyrosine protein kinase B (TrkB). Mechanistically, the inhibitory effects of ICS II were abrogated by Rp-8-Br-cGMP (a PKG inhibitor) or ANA-12 (a TrkB inhibitor), which further confirmed that the favorable effects of ICS II were attributed to its activation of the PKG/CREB/BDNF signaling pathways. Intriguingly, ICS II might effectively bind and inhibited PDE5 activity as demonstrated by relatively high binding scores (-6.52 kcal/mol).

Conclusions: ICS II significantly rescues OGD/R-induced hippocampal neuronal injury. The mechanism is, at least partly, due to inhibition of PDE5 and activation of PKG/CREB/BDNF/TrkB signaling pathway. Hence it is thought that ICS II might be a potential naturally PDE5 inhibitor to combat cerebral I/R injury.
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http://dx.doi.org/10.3389/fphar.2020.00523DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7194126PMC
April 2020

Icariin protects against sodium azide-induced neurotoxicity by activating the PI3K/Akt/GSK-3β signaling pathway.

PeerJ 2020 20;8:e8955. Epub 2020 Apr 20.

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, China.

Background: Icariin (ICA) is one of the major active flavonoids extracted from the traditional Chinese herb Maxim and has been shown to have neuroprotective effects. This study was designed to investigate the effect of ICA on sodium azide (NaN)-induced rat adrenal pheochromocytoma (PC12) cell damage and to further examine the underlying mechanisms.

Methods: To explore its possible mechanism, we used NaN (50 mM)-induced neuronal PC12 cell damage. Cell viability was evaluated by CCK-8 and lactate dehydrogenase (LDH) assays. Mitochondrial membrane potential (MMP) was detected by JC-1. Glucose concentration was assessed by the glucose oxidase method. The role of ICA in the PI3K/Akt/GSK-3β signaling pathway was explored by Western blotting.

Results: The results indicate that pretreatment with ICA reduced NaN-induced cell damage and significantly reduced the leakage rate of LDH in PC12 cells. ICA pretreatment increased the MMP and a decrease in glucose concentration indicate increased glucose consumption. Furthermore, the protein levels of p-PI3K (p85), PI3K-110α, p-Ser473-Akt and p-Ser9-GSK-3β were markedly decreased in PC12 cells after NaN treatment for 24 h, whereas these effects were reverted after pretreatment with ICA. Tau phosphorylation at the Ser396/404 and Thr217 sites was significantly decreased by pretreatment with ICA.

Conclusions: These results suggest that ICA protects against NaN-induced neurotoxicity in PC12 cells by activating the PI3K/Akt/GSK-3β signaling pathway.
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http://dx.doi.org/10.7717/peerj.8955DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7179568PMC
April 2020

New Insights into Detection of a Dendrobine Compound From a Novel Endophytic Strain and Its Toxicity Against Phytopathogenic Bacteria.

Front Microbiol 2020 12;11:337. Epub 2020 Mar 12.

Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi, China.

is the only plant that could produce the natural bioactive dendrobine. No other source of dendrobine has been found to date except from and via chemical synthesis. In this study, we aimed to examine the potential fungal endophyte isolated from stem segments using the molecular method and to detect dendrobine compound through high-performance liquid chromatography (HPLC), gas chromatography-mass spectrometry (GC-MS), and liquid chromatography with tandem mass spectrometry (LC-MS/MS) and their metabolite for their antibacterial activity. The potential dendrobine producer strain was recognized as based on molecular DNA sequencing and GenBank databases. The MD33 produced dendrobine and other compounds in a potato dextrose medium (PDM), as confirmed by HPLC retention time peak analysis. The HPLC results revealed that MD33 biomass showed a peak retention time of 5.28 ± 0.2 min, similar to wild stem dendrobine (5.32 ± 0.2 min) and standard chemical reference dendrobine (5.30 ± 0.2 min), indicating the presence of dendrobine in the fungal biomass. Results of GC-MS and LC-MS analysis revealed that MD33 produced the same molecular weight (263 in GC-MS and 264.195 in LC-MS) of dendrobine as compared with standard chemical reference dendrobine and dendrobine. Antibacterial activity data revealed that MD33 produced the strongest bactericidal activity against , , and species, and the diameter of the bacterial growth inhibition zone was 12 ± 0.2, 9 ± 0.2, and 8 ± 0.2 mm, respectively. To the best of our knowledge, this was the first study to investigate as a dendrobine producer, and the results revealed that was directly involved in the potential production of a similar bioactive compound to (dendrobine). In addition, the metabolite exhibited potent antibacterial activity and can be a potential strain for medical and industrial purposes.
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http://dx.doi.org/10.3389/fmicb.2020.00337DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7080861PMC
March 2020

Neuroprotective Effects of Trilobatin, a Novel Naturally Occurring Sirt3 Agonist from Rehd., Mitigate Cerebral Ischemia/Reperfusion Injury: Involvement of TLR4/NF-κB and Nrf2/Keap-1 Signaling.

Antioxid Redox Signal 2020 07 23;33(2):117-143. Epub 2020 Apr 23.

Department of Clinical Pharmacotherapeutics, School of Pharmacy, Zunyi Medical University, Zunyi, China.

Neuroinflammation and oxidative stress are deemed the prime causes of brain injury after cerebral ischemia/reperfusion (I/R). Since the silent mating-type information regulation 2 homologue 3 (Sirt3) pathway plays an imperative role in protecting against neuroinflammation and oxidative stress, it has been verified as a target to treat ischemia stroke. Therefore, we attempted to seek novel Sirt3 agonist and explore its underlying mechanism for stroke treatment both and . Trilobatin (TLB) not only dramatically suppressed neuroinflammation and oxidative stress injury after middle cerebral artery occlusion in rats, but also effectively mitigated oxygen and glucose deprivation/reoxygenation injury in primary cultured astrocytes. These beneficial effects, along with the reduced proinflammatory cytokines suppressing Toll-like receptor 4 (TLR4) signaling pathway, lessened oxidative injury activating nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways, in keeping with the findings . Intriguingly, the TLB-mediated neuroprotection on cerebral I/R injury was modulated by reciprocity between TLR4-mediated neuroinflammatory responses and Nrf2 antioxidant responses as evidenced by molecular docking and silencing TLR4 and Nrf2, respectively. Most importantly, TLB not only directly bonded to Sirt3 but also increased Sirt3 expression and activity, indicating that Sirt3 might be a promising therapeutic target of TLB. TLB is a naturally occurring Sirt3 agonist with potent neuroprotective effects regulation of TLR4/nuclear factor-kappa B and Nrf2/Kelch-like ECH-associated protein 1 (Keap-1) signaling pathways both and . Our findings indicate that TLB protects against cerebral I/R-induced neuroinflammation and oxidative injury through the regulation of neuroinflammatory and oxidative responses TLR4, Nrf2, and Sirt3, suggesting that TLB might be a promising Sirt3 agonist against ischemic stroke.
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http://dx.doi.org/10.1089/ars.2019.7825DOI Listing
July 2020

Pharmacological effects of icariin.

Adv Pharmacol 2020 13;87:179-203. Epub 2020 Jan 13.

Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, P.R. China; Generic Drug Research Center of Guizhou Province, School of Pharmacy, Zunyi Medical University, Zunyi, Guizhou, P.R. China. Electronic address:

Icariin (ICA) is a principal active component from traditional Chinese medicine Epimedium grandiflorum. To explain its traditional medical usages by modern science, a variety of pharmacological effects have been studied for ICA. In this review, we summarized the pharmacokinetics of ICA as well as its pharmacological mechanisms in neurodegenerative disease, cardiovascular disease, anti-osteoporosis, anti-inflammation, anti-oxidative stress, anti-depression and anti-tumors.
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http://dx.doi.org/10.1016/bs.apha.2019.10.004DOI Listing
June 2020

ROCK1 activation-mediated mitochondrial translocation of Drp1 and cofilin are required for arnidiol-induced mitochondrial fission and apoptosis.

J Exp Clin Cancer Res 2020 Feb 19;39(1):37. Epub 2020 Feb 19.

College of Pharmacy, Army Medical University, 30 Gaotanyan Street, Shapingba District, Chongqing, 400038, China.

Background: Arnidiol is a pentacyclic triterpene diol that has multiple pharmacological activities. However, the apoptotic activities of arnidiol in human cancer cells have not yet been explored, nor has the mechanism by which arnidiol induces apoptosis been examined in depth.

Methods: MDA-MB-231 cells and xenografted mice were treated with arnidiol. Mitochondrial fission and apoptosis were determined by immunofluorescence, flow cytometry and related molecular biological techniques. The interaction and colocalization of cofilin and Drp1 was determined by immunoprecipitation and immunofluorescence assays.

Results: Arnidiol induces mitochondrial fission and apoptosis through mitochondrial translocation of Drp1 and cofilin. Importantly, the interaction of Drp1 and cofilin in mitochondria is involved in arnidiol-induced mitochondrial fission and apoptosis. Knockdown of either Drp1 or cofilin abrogated arnidiol-induced mitochondrial translocation, interaction of Drp1 and cofilin, mitochondrial fission and apoptosis. Only dephosphorylated Drp1 (Ser637) and cofilin (Ser3) were translocated to the mitochondria. Mutants of Drp1 S637A and cofilin S3A, which mimic the dephosphorylated forms, enhanced mitochondrial fission and apoptosis induced by arnidiol, whereas mutants of Drp1 S637D and cofilin S3E, which mimic the phosphorylated forms, suppressed mitochondrial fission and apoptosis induced by arnidiol. A mechanistic study revealed that ROCK1 activation plays an important role in the arnidiol-mediated Drp1 and cofilin dephosphorylation and mitochondrial translocation, mitochondrial fission, and apoptosis.

Conclusions: Our data reveal a novel role of both Drp1 and cofilin in the regulation of mitochondrial fission and apoptosis and suggest that arnidiol could be developed as a potential agent for the treatment of human cancer.
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http://dx.doi.org/10.1186/s13046-020-01545-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031977PMC
February 2020

Molecular Identification of Endophytic Fungi and Their Pathogenicity Evaluation Against and .

Int J Mol Sci 2020 Jan 2;21(1). Epub 2020 Jan 2.

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi 563003, China.

are tropical orchid plants that host diverse endophytic fungi. The role of these fungi is not currently well understood in plants. We morphologically and molecularly identified these fungal endophytes, and created an efficient system for evaluating the pathogenicity and symptoms of endophytic fungi on and though in vitro co-culturing. ReThe colony morphological traits of myco-endophytes (DMEs) were recorded for their identification. Molecular identification revealed the presence of Colletotrichum tropicicola, Fusarium keratoplasticum, Fusarium oxysporum, Fusarium solani, and Trichoderma longibrachiatum. The pathogenicity results revealed that T. longibrachiatum produced the least pathogenic effects against D. nobile protocorms. In seedlings, T. longibrachiatum showed the least pathogenic effects against D. officinale seedlings after seven days. C. tropicicola produced highly pathogenic effects against both Dendrobium seedlings. The results of histological examination of infected tissues revealed that F. keratoplasticum and T. longibrachiatum fulfill Koch's postulates for the existence of endophytes inside the living tissues. The DMEs are cross-transmitted inside the host plant cells, playing an important role in plant host development, resistance, and alkaloids stimulation.
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http://dx.doi.org/10.3390/ijms21010316DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6982089PMC
January 2020

CZYH Alleviates -Amyloid-Induced Cognitive Impairment and Inflammation Response via Modulation of JNK and NF-B Pathway in Rats.

Behav Neurol 2019 4;2019:9546761. Epub 2019 Nov 4.

Key Laboratory of Basic Pharmacology of Ministry of Education, Department of Pharmacology, Zunyi Medical University, Zunyi, Guizhou 563000, China.

Cu-Zhi-Yi-Hao (CZYH), an empirical formula of traditional Chinese medicine (TCM), has been used for amnesia treatment in clinical practice. However, its underlying pharmacological mechanism has not been fully illuminated. The current study was designed to investigate the neuroprotective effect of CZYH on a -amyloid 25-35- (A-) induced learning and memory deficit rat model. CZYH (200, 400, or 800 mg/kg), donepezil (1.0 mg/kg), or distilled water was given to A-stimulated animals for 17 days consecutively. The Morris water maze test revealed that CZYH (400 or 800 mg/kg) administration improved the A-induced cognitive impairments in rats, and Nissl staining demonstrated that CZYH mitigated the A-caused neuron loss. In addition, CZYH treatment markedly inhibited the activation of microglia as evidenced by a decreased level of IBA-1 and increased YM-1/2 protein expression. The protein expression levels of TNF-, IL-1, and COX-2 were also repressed by CZYH. Besides, CZYH treatment alleviated A-induced IB- degradation and NF-B p65 phosphorylation, as well as reduced the JNK phosphorylation level. In conclusion, the present study suggests that CZYH could improve learning and memory abilities and relieve neuron loss in A-induced rats, at least partly through inhibition of the neuroinflammatory response via inhibiting the JNK-dependent NF-B activation, indicating that CZYH might be a promising formula for the treatment of AD.
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http://dx.doi.org/10.1155/2019/9546761DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6875391PMC
April 2020

Icariside II, a phosphodiesterase 5 inhibitor, attenuates cerebral ischaemia/reperfusion injury by inhibiting glycogen synthase kinase-3β-mediated activation of autophagy.

Br J Pharmacol 2020 03 16;177(6):1434-1452. Epub 2020 Feb 16.

Department of Pharmacology, Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, P. R. China.

Background And Purpose: Cerebral ischaemia/reperfusion causes exacerbated neuronal damage involving excessive autophagy and neuronal loss. The present study was designed to investigate the effect of icariside II, one of main active ingredients of Herba Epimedii on this loss and whether this is related to its PDE 5 inhibitory action.

Experimental Approach: Focal cerebral ischaemia was induced in the rat by transient middle cerebral artery occlusion over 2 hr, followed by reperfusion with icariside II, 3-methylamphetamine or rapamycin. The effect of icariside II was determined measuring behaviour changes and the size of the infarction. The expressions of PDE 5, autophagy-related proteins and the level of phosphorylation of glycogen synthase kinase-3β (GSK-3β) were determined. Cultured primary cortical neurons were subjected to oxygen and glucose deprivation followed by reoxygenation in the presence and absence of icariside II. A surface plasmon resonance assay and molecular docking were used to explore the interactions of icariside II with PDE 5 or GSK-3β.

Key Results: Icariside II not only protected against induced ischaemic reperfusion injury in rats but also attenuated such injury in primary cortical neurons. The neuroprotective effects of icariside II on such injury were attributed to interfering with the PKG/GSK-3β/autophagy axis by directly bounding to PDE 5 and GSK-3β.

Conclusions And Implications: These findings indicate that icariside II attenuates cerebral I/R-induced injury via interfering with PKG/GSK-3β/autophagy axis. This study raises the possibility that icariside II and other PDE 5 inhibitors maybe effective in the treatment ischaemia stroke.
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http://dx.doi.org/10.1111/bph.14912DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7056470PMC
March 2020

Bioengineering tools for the production of pharmaceuticals: current perspective and future outlook.

Bioengineered 2019 12;10(1):469-492

Bioresource Institute for Healthy Utilization, Zunyi Medical University , Zunyi , China.

The bioengineering tools have significant advantages through less time-consuming and utilized as a promising stage for the production of pharmaceutical bioproducts under the single platform. This review highlighted the advantages and current improvement in the plant, animal and microbial bioengineering tools and outlines feasible approaches by biological and process's bioengineering levels for advancing the economic feasibility of pharmaceutical's production. The critical analysis results revealed that system biology and synthetic biology along with advanced bioengineering tools like transcriptome, proteome, metabolome and nano bioengineering tools have shown a promising impact on the development of pharmaceutical's bioproducts. Tools to overcome and resolve the accompanying encounters of pharmaceutical's production that include nano bioengineering tools are also discussed. As a summary and prospect, it also gives new insight into the challenges and possible breakthrough of the development of pharmaceutical's bioproducts through bioengineering tools.
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http://dx.doi.org/10.1080/21655979.2019.1682108DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6844412PMC
December 2019

alkaloids decrease Aβ by regulating α- and β-secretases in hippocampal neurons of SD rats.

PeerJ 2019 6;7:e7627. Epub 2019 Sep 6.

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, China.

Background: Alzheimer's disease (AD) is the primary cause of dementia in the elderly. The imbalance between production and clearance of amyloid β (Aβ) is a very early, often initiating factor in AD. Lindl. alkaloids (DNLA) extracted from a Chinese medicinal herb, which have been shown to have anti-aging effects, protected against neuronal impairment and . Moreover, we confirmed that DNLA can improve learning and memory function in elderly normal mice, indicating that DNLA has potential health benefits. However, the underlying mechanism is unclear. Therefore, we further explored the effect of DNLA on neurons, which is closely related to learning and memory, based on Aβ.

Methods: We exposed cultured hippocampal neurons to DNLA to investigate the effect of DNLA on Aβ . Cell viability was evaluated by MTT assays. Proteins were analyzed by Western blot analysis.

Results: The cell viability of hippocampal neurons was not changed significantly after treatment with DNLA. But DNLA reduced the protein expression of amyloid precursor protein (APP), disintegrin and metalloprotease 10 (ADAM10), β-site APP cleaving enzyme 1 (BACE1) and Aβ of hippocampal neurons in rats and increased the protein expression of ADAM17.

Conclusions: DNLA decreases Aβ by regulating α- and β-secretase in hippocampal neurons of SD rats.
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http://dx.doi.org/10.7717/peerj.7627DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733236PMC
September 2019

A review of plant leaf fungal diseases and its environment speciation.

Bioengineered 2019 12;10(1):409-424

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University , Zunyi , Guizhou , China.

There is increasing difficulty in identifying new plant leaf diseases as a result of environmental change. There is a need to identify the factors influencing the emergence and the increasing incidences of these diseases. Here, we present emerging fungal plant leaf diseases and describe their environmental speciation. We considered the factors controlling for local adaptation associated with environmental speciation. We determined that the advent of emergent fungal leaf diseases is closely connected to environmental speciation. Fungal pathogens targeting the leaves may adversely affect the entire plant body. To mitigate the injury caused by these pathogens, it is necessary to be able to detect and identify them early in the infection process. In this way, their distribution, virulence, incidence, and severity could be attenuated.
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http://dx.doi.org/10.1080/21655979.2019.1649520DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6779379PMC
December 2019

New insights and rethinking of cinnabar for chemical and its pharmacological dynamics.

Bioengineered 2019 12;10(1):353-364

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University , Guizhou , China.

Cinnabar is an attractive mineral with many different uses. It is reported that cinnabar is one of the traditional Chinese's medicines extensively use. The main objective of this critical review is to identify the current overview, concept and chemistry of cinnabar, which includes the process developments, challenges, and diverse options for pharmacology research. It is used as a medicine through probable toxicity, especially when taking overdoes. This review is the first to describe the toxicological effects of cinnabar and its associated compounds. Nuclear magnetic resonance (NMR) dependent metabolomics could be useful for examination of the pharmaceutical consequence. The analysis indicated that the accurate preparation methods, appropriate doses, disease status, ages with drug combinations are significant factors for impacting the cinnabar toxicity. Toxicologically, synthetic mercury sulfide or cinnabar should be notable for mercuric chloride, mercury vapor and methyl mercury for future protection and need several prominent advancements in cinnabar research.
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http://dx.doi.org/10.1080/21655979.2019.1652491DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6738451PMC
December 2019

Icariin improves the cognitive function of APP/PS1 mice via suppressing endoplasmic reticulum stress.

Life Sci 2019 Oct 7;234:116739. Epub 2019 Aug 7.

Key Laboratory of Basic Pharmacology of Ministry of Education, Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, China.

Aim: This study aimed to investigate the effect of icariin (referred as ICA) on Alzheimer's disease (AD) model through endoplasmic reticulum (ER) stress pathway.

Main Methods: Nine months male APP/PS1 and wild-type (WT) mice were randomly divided into four groups: APP/PS1 control, APP/PS1 + ICA, WT control and WT + ICA groups. The treated mice were given ICA 60 mg/kg/d and control mice were received the same volume distilled water for consecutive 3 months. The Morris water maze and Novel object recognition were used to detect animals' behavior. Nissl staining was used to observe the neuronal morphology in hippocampus area. Aβ deposition in hippocampal region was observed by immunofluorescence staining. TUNEL staining was used to observe apoptosis. Detection of expression of ER stress related factors by Western blot and real time RT-PCR.

Key Findings: Chronically administrated with ICA compared with APP/PS1 control mice significantly improved the behavior performance, reduced neuronal apoptosis, as well as suppressing the ER stress signaling pathway, including that decreased the level of glucose-regulated protein 78, phosphorylated ER-regulated kinase and phosphorylated eukaryotic initiation factor α, as well activating transcription factor-4, C/EBP homologous protein, DNA damage inducible protein 34 and tribbles homologous protein 3.

Significance: Our data indicated that ICA suppressed the ER stress signaling to protect against AD animal model, these findings suggest that a potential point for researching the effect of ICA on neurodegeneration.
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http://dx.doi.org/10.1016/j.lfs.2019.116739DOI Listing
October 2019

Microbial dynamics for lignocellulosic waste bioconversion and its importance with modern circular economy, challenges and future perspectives.

Bioresour Technol 2019 Nov 27;291:121905. Epub 2019 Jul 27.

Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi 563003, China.

An extensive use of microbial dynamics for utilizing the lignocellulosic wastes has been attributed to their efficiency in bioenergy and bioproducts development as a cost effective high nutritional value. The integration of lignocellulosic waste into the circular economy can scaleup the sustainable bioproducts and bioenergy development. In this review paper, the aim is to describe the existing research efforts on organic lignocellulosic waste, cellulase producing microbes, their potential enzyme, modern circular economy with associated challenges and future perspectives. Presently, it has been reviewed that microbial cellulases have provided treasure bioproducts visions into industrial bioproducts marvels unveiled through lignocellulosic waste cutting-edge microbial explorations. Furthermore, the review focused on new insights of the growing circular economy of lignocellulosic waste used for many bioproducts and bioenergy dealings and explored the emergent lignocellulosic biorefinery approaches which could then be applied to review industrial-scale sustainable economic models for upgraded bioproducts and other production associated problems.
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http://dx.doi.org/10.1016/j.biortech.2019.121905DOI Listing
November 2019