Publications by authors named "Ziru Dai"

13 Publications

  • Page 1 of 1

Corrigendum: Ginsenoside Re Attenuates High Glucose-Induced RF/6A Injury Regulating PI3K/AKT Inhibited HIF-1a/VEGF Signaling Pathway.

Front Pharmacol 2020 23;11:1312. Epub 2020 Oct 23.

Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.

[This corrects the article DOI: 10.3389/fphar.2020.00695.].
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http://dx.doi.org/10.3389/fphar.2020.01312DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7645230PMC
October 2020

Intestinal Tract Microbe Communities Associated with Horseshoe Crabs from Beibu Gulf, China.

Curr Microbiol 2020 Nov 14;77(11):3330-3338. Epub 2020 Sep 14.

Guangxi Key Laboratory of Beibu Gulf Marine Biodiversity Conservation, Beibu Gulf University, Qinzhou, 535011, Guangxi, China.

Until now, there has been little research on the intestinal microbial community of horseshoe crabs. To fill this gap, we investigated the microbiome composition of the Chinese horseshoe crab, Tachypleus tridentatus, and the mangrove horseshoe crab, Carcinoscorpius rotundicauda. We sequenced the 16S rRNA gene of intestinal bacterial species and compared the microbial community structure and diversity. Next, we show that the total effective bacterial sequence was 36,865 reads, and the average annotated operational taxonomic unit (OTU) number was 240. Through hierarchical clustering analysis and principal coordinate analysis samples from two horseshoe crab species, we found that the intestinal flora of the same horseshoe crab species was relatively concentrated, while the microbiome of a different horseshoe crab species were significantly separated. Cluster analysis showed that two samples, one from Chinese horseshoe crabs and one from mangrove horseshoe crabs, had similar microbial community structure, while other samples were relatively discrete. The gut microbiota of the mangrove horseshoe crab were dominated by the phyla Tenericutes (42.71%), Firmicutes (24.27%), and Proteobacteria (20.39%), while the top three phyla in the Chinese horseshoe crab intestinal tract were Tenericutes (57.19%), Proteobacteria (22.14%), and Bacteroidetes (7.38%). To intuitively understand the similarity and overlap of the OTU composition of each group, we performed Venn diagram analysis. The two species shared 284 OTUs, accounting for 81.8% of the total. This indicates that although there is high similarity between mangrove and Chinese horseshoe crab in gastrointestinal microbial community structure, there are also some differences, which deserve further discussion.
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http://dx.doi.org/10.1007/s00284-020-02140-xDOI Listing
November 2020

Corrigendum to "Ginsenoside Rb1 and mitochondria: A short review of the literature" [Mol. Cell. Probe (43) 2019 1-5].

Mol Cell Probes 2020 Dec 2;54:101626. Epub 2020 Sep 2.

Institute of Medicinal Plant Development, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100193, China. Electronic address:

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http://dx.doi.org/10.1016/j.mcp.2020.101626DOI Listing
December 2020

Ginsenoside Re Attenuates High Glucose-Induced RF/6A Injury Regulating PI3K/AKT Inhibited HIF-1α/VEGF Signaling Pathway.

Front Pharmacol 2020 21;11:695. Epub 2020 May 21.

Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.

Hyperglycaemia-induced retinal microvascular endothelial cell apoptosis is a critical and principle event in diabetic retinopathy (DR), which involves a series of complex processes such as mitochondrial dysfunction and oxidative stress. Ginsenoside Re (Re), a key ingredients of ginseng, is considered to have various pharmacologic functions, such as antioxidative, inhibition of inflammation and anti-apoptotic properties. However, the effects of Re in DR and the related mechanisms of endothelial cell injury induced by high glucose (HG) exposure remain unclear. The present study was designed to investigate and evaluate the ability of Re to ameliorate HG-induced retinal endothelial RF/6A cell injury and the potential mechanisms involved in the hypoxia-inducible factor-1-alpha (HIF-1α)/vascular endothelial growth factor (VEGF) signaling regulated by phosphoinositide 3-kinase (PI3K)/AKT pathway. Our results showed that preincubation with Re exerted cytoprotective effects by reversing the HG-induced decrease in RF/6A cell viability, downregulation of apoptosis rate and inhibition of oxidative-related enzymes, thereby reducing the excess intracellular reactive oxygen species (ROS) and HG-triggered RF/6A cell injury. In addition, Western blot analysis results showed ginsenoside Re significantly increased HIF-1α expression in the cytoplasm but decreased its expression in the nucleus, suggesting that it reduced the translocation of HIF-1α from the cytoplasm to the nucleus, and downregulated VEGF level. Moreover, this effect is involved in the activation of the PI3K/Akt pathway. LY294002, a PI3K inhibitor, was used to block the Akt pathway. Afterwards, the effects of Re on the regulation of apoptotic related proteins, VEGF and HIF-1α nuclear transcription was partially reversed. These findings suggested the exerting protective effects of ginsenoside Re were associated with regulating of PI3K/AKT and HIF-1α/VEGF signaling pathway, which indicates that ginsenoside Re may ameliorates HG-induced retinal angiogenesis and suggests the potential for the development of Re as a therapeutic for DR.
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http://dx.doi.org/10.3389/fphar.2020.00695DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253708PMC
May 2020

Interspecies Variation in NCMNDemethylation in Liver Microsomes from Various Species.

Molecules 2019 Jul 30;24(15). Epub 2019 Jul 30.

Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

NCMN (-(3-carboxy propyl)-4-methoxy-1,8-naphthalimide), a newly developed ratiometric two-photon fluorescent probe for human Cytochrome P450 1A (CYP1A), shows the best combination of specificity and reactivity for real-time detection of the enzymatic activities of CYP1A in complex biological systems. This study aimed to investigate the interspecies variation in NCMNdemethylation in commercially available liver microsomes from human, mouse, rat, beagle dog, minipig and cynomolgus monkey. Metabolite profiling demonstrated that NCMN could be -demethylated in liver microsomes from all species but the reaction rate varied considerably. CYP1A was the major isoform involved in NCMNdemethylation in all examined liver microsomes based on the chemical inhibition assays. Furafylline, a specific inhibitor of mammalian CYP1A, displayed differential inhibitory effects on NCMNdemethylation in all tested species. Kinetic analyses demonstrated that NCMNdemethylation in liver microsomes form rat, minipig and cynomolgus monkey followed biphasic kinetics, while in liver microsomes form human, mouse and beagle dog obeyed Michaelis-Menten kinetics, the kinetic parameters from various species are much varied, while NCMNdemethylation in MLM exhibited the highest similarity of specificity, kinetic behavior and intrinsic clearance as that in HLM. These findings will be very helpful for the rational use of NCMN as a practical tool to decipher the functions of mammalian CYP1A or to study CYP1A associated drug-drug interactions .
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http://dx.doi.org/10.3390/molecules24152765DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6695839PMC
July 2019

Corrigendum: Depletion of Myostatin b Promotes Somatic Growth and Lipid Metabolism in Zebrafish.

Front Endocrinol (Lausanne) 2019 22;10:332. Epub 2019 May 22.

Key Laboratory of Aquatic Biodiversity and Conservation, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.

[This corrects the article DOI: 10.3389/fendo.2016.00088.].
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http://dx.doi.org/10.3389/fendo.2019.00332DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6540931PMC
May 2019

Protective Effects of Total Saponins of (Miq.) on Endothelial Cell Injury Induced by TNF-α via Modulation of the PI3K/Akt and NF-κB Signalling Pathways.

Int J Mol Sci 2018 Dec 21;20(1). Epub 2018 Dec 21.

Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, China.

Atherosclerosis is an arterial disease associated with inflammation. Hence, the discovery of novel therapeutic agents for suppressing inflammatory responses is urgent and vital for the treatment of atherosclerosis in cardiovascular diseases. The total saponins of (Miq.) Seem. (TAS) are the main components extracted from the Chinese traditional herb Longya L., a folk medicine used in Asian countries for treating numerous diseases, enhancing energy and boosting immunity. However, the protective effects of TAS against inflammation-triggered vascular endothelial dysfunction, a critical early event during the course of atherosclerosis, and the potential mechanisms of this protection have been not demonstrated. Accordingly, the aim of this study was to investigate the anti-inflammatory and anti-apoptotic effects and the protective mechanisms of TAS, and show how TAS ameliorates human umbilical vein endothelial cell (HUVEC) damage caused by tumour necrosis factor-α (TNF-α). The results indicated that TAS exerted cytoprotective effects by inhibiting TNF-α-triggered HUVEC apoptosis, mitochondrial membrane potential depolarisation, and the regulation of inflammatory factors (IL-6, MCP-1, and VCAM-1) while suppressing NF-κB transcription. Furthermore, this phenomenon was related to activation of the phosphoinositide 3-kinase (PI3K)/Akt signalling pathway. Blocking the Akt pathway with LY294002, a PI3K inhibitor, reversed the cytoprotective effect of TAS against TNF-α-induced endothelial cell death. Moreover, LY294002 partially abolished the effects of TAS on the upregulation of the Bcl-2 family of proteins and the downregulation of Bax protein expression. In conclusion, the results of our study suggest that TAS suppresses the inflammation and apoptosis of HUVECs induced by TNF-α and that PI3K/Akt signalling plays a key role in promoting cell survival and anti-inflammatory reactions during this process.
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http://dx.doi.org/10.3390/ijms20010036DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6337668PMC
December 2018

Protective Effects and Target Network Analysis of Ginsenoside Rg1 in Cerebral Ischemia and Reperfusion Injury: A Comprehensive Overview of Experimental Studies.

Cells 2018 Dec 12;7(12). Epub 2018 Dec 12.

Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, China.

Cerebral ischemia-reperfusion is a complicated pathological process. The injury and cascade reactions caused by cerebral ischemia and reperfusion are characterized by high mortality, high recurrence, and high disability. However, only a limited number of antithrombotic drugs, such as recombinant tissue plasminogen activator (r-TPA), aspirin, and heparin, are currently available for ischemic stroke, and its safety concerns is inevitable which associated with reperfusion injury and hemorrhage. Therefore, it is necessary to further explore and examine some potential neuroprotective agents with treatment for cerebral ischemia and reperfusion injury to reduce safety concerns caused by antithrombotic drugs in ischemic stroke. Ginseng Rg1 (G-Rg1) is a saponin composed of natural active ingredients and derived from the roots or stems of and ginseng in traditional Chinese medicine. Its pharmacological effects exert remarkable neurotrophic and neuroprotective effects in the central nervous system. To explore and summarize the protective effects and mechanisms of ginsenoside Rg1 against cerebral ischemia and reperfusion injury, we conducted this review, in which we searched the PubMed database to obtain and organize studies concerning the pharmacological effects and mechanisms of ginsenoside Rg1 against cerebral ischemia and reperfusion injury. This study provides a valuable reference and clues for the development of new agents to combat ischemic stroke. Our summarized review and analysis show that the pharmacological effects of and mechanisms underlying ginsenoside Rg1 activity against cerebral ischemia and reperfusion injury mainly involve 4 sets of mechanisms: anti-oxidant activity and associated apoptosis via the Akt, Nrf2/HO-1, PPARγ/HO-1, extracellular regulated protein kinases (ERK), p38, and c-Jun N-terminal kinase (JNK) pathways (or mitochondrial apoptosis pathway) and the caspase-3/ROCK1/MLC pathway; anti-inflammatory and immune stimulatory-related activities that involve apoptosis or necrosis via MAPK pathways (the JNK1/2 + ERK1/2 and PPARγ/HO-1 pathways), endoplasmic reticulum stress (ERS), high mobility group protein1 (HMGB1)-induced TLR2/4/9 and receptor for advanced glycation end products (RAGE) pathways, and the activation of NF-κB; neurological cell cycle, proliferation, differentiation, and regeneration via the MAPK pathways (JNK1/2 + ERK1/2, PI3K-Akt/mTOR, PKB/Akt and HIF-1α/VEGF pathways); and energy metabolism and the regulation of cellular ATP levels, the blood-brain barrier and other effects via N-methyl-D-aspartic acid (NMDA) receptors, ERS, and AMP/AMPK-GLUT pathways. Collectively, these mechanisms result in significant neuroprotective effects against cerebral ischemic injury. These findings will be valuable in that they should further promote the development of candidate drugs and provide more information to support the application of previous findings in stroke clinical trials.
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http://dx.doi.org/10.3390/cells7120270DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6316103PMC
December 2018

Ginsenoside Rb1 and mitochondria: A short review of the literature.

Mol Cell Probes 2019 02 4;43:1-5. Epub 2018 Dec 4.

Institute of Medicinal Plant Development, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100193, China. Electronic address:

Mitochondria play a central role in various critical cellular processes, including energy synthesis, energy supply and apoptosis. Panax notoginseng, a commonly used traditional Chinese medicine, has various pharmacological effects on the human body. Ginsenosides are representative bioactive components of P. notoginseng. Recently, more attention has focused on ginsenoside Rb1 as an antioxidative and anti-inflammatory agent that can protect the nervous system and the cardiovascular system. Numerous studies have shown that Rb1 exerts these effects by regulating mitochondrial energy metabolism, mitochondrial fission and fusion, apoptosis, oxidative stress and reactive oxygen species release, mitophagy and mitochondrial membrane potential. Thus, the mitochondria are pivotal targets of Rb1. This review summarized the available reports of the effects of ginsenoside Rb1 on the regulation of mitochondria and showed that it has a promising role in treating mitochondrial diseases.
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http://dx.doi.org/10.1016/j.mcp.2018.12.001DOI Listing
February 2019

Inhibitory Effects of Ginsenoside Rb1 on Early Atherosclerosis in ApoE-/- Mice via Inhibition of Apoptosis and Enhancing Autophagy.

Molecules 2018 Nov 8;23(11). Epub 2018 Nov 8.

Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, China.

Inflammation is a major contributing factor to the progression of atherosclerosis. Ginsenoside Rb1 (Rb1), an active saponin of , has been found to exert beneficial effects on inflammation and oxidative stress. This study investigated the ability of Rb1 to inhibit the formation of atherosclerotic plaques and the potential mechanisms. In this study, the effects of Rb1 on the development of atherosclerosis were investigated in ApoE-/- deficient mice fed with a western diet. Mice were intragastrically administrated with Rb1 (10 mg/kg) for 8 weeks. This study is that ginsenoside Rb1 exerted an inhibitory effect on early atherosclerosis in ApoE-/- mice via decreasing body weight and food intake daily, upregulating the lipid levels of serum plasma, including those of TC, TG and LDL-C and HDL-C and reducing the atherosclerotic plaque area, suppressing inflammatory cytokines (levels of IL-1β, IL-6 and TNF-α) in the serum of ApoE-/- mice, changing the expression levels of BCL-2, BAX, cleaved caspase-3 and cleaved caspase-9 and weakening apoptosis associated with anti-inflammatory activity. Hence, all these effects against atherosclerosis were tightly associated with regulation of necrosis or apoptosis associated with anti-inflammatory activity. Additionally, the results found that ginsenoside Rb1 increased autophagy flux to inhibit apoptosis via acceleration of autophagy by promoting transformation of LC3 from type I to type II in high-fat diet-induced atherosclerosis in ApoE-/- mice. This finding, along with those of the previous study, provides evidence that Rb1 promotes the process of autophagy to protect against atherosclerosis via regulating BCL-2 family-related apoptosis. These results indicate that Rb1 exhibits therapeutic effects in atherosclerosis by reversing the imbalance between apoptosis and autophagy.
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http://dx.doi.org/10.3390/molecules23112912DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6278435PMC
November 2018

Depletion of Myostatin b Promotes Somatic Growth and Lipid Metabolism in Zebrafish.

Front Endocrinol (Lausanne) 2016 4;7:88. Epub 2016 Jul 4.

Key Laboratory of Development and High-Value Utilization of Beibu Gulf Seafood Resource, Guangxi Key Laboratory of Beibu Gulf Marine Biodiversity Conservation, College of Food Engineering, Qinzhou University, Qinzhou, China

Myostatin (MSTN) is a negative regulator of myogenesis in vertebrates. Depletion of mstn resulted in elevated muscle growth in several animal species. However, the report on the complete ablation of mstn in teleost fish has not yet become available. In this study, two independent mstnb-deficient mutant lines in zebrafish were generated with the TALENs technique. In the mstnb-deficient zebrafish, enhanced muscle growth with muscle fiber hyperplasia was achieved. Beginning at the adult stage (80 days postfertilization), the mstnb-deficient zebrafish exhibited increased circumferences and body weights compared with the wild-type sibling control fish. Although the overall total lipid/body weight ratios remained similar between the mstnb-deficient zebrafish and the control fish, the distribution of lipids was altered. The size of the visceral adipose tissues became smaller while more lipids accumulated in skeletal muscle in the mstnb-deficient zebrafish than in the wild-type control fish. Based on the transcriptional expression profiles, our results revealed that lipid metabolism, including lipolysis and lipogenesis processes, was highly activated in the mstnb-deficient zebrafish, which indicated the transition of energy metabolism from protein-dependent to lipid-dependent in mstnb-deficient zebrafish. Our mstnb-deficient model could be valuable in understanding not only the growth trait regulation in teleosts but also the mechanisms of teleost energy metabolism.
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http://dx.doi.org/10.3389/fendo.2016.00088DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4930940PMC
July 2016

The basal function of teleost prolactin as a key regulator on ion uptake identified with zebrafish knockout models.

Sci Rep 2016 Jan 4;6:18597. Epub 2016 Jan 4.

Key Laboratory of Aquatic Biodiversity and Conservation of the Chinese Academy of Sciences, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, Hubei, 430072, China.

Prolactin (PRL) is an anterior pituitary hormone with a broad range of functions. Its ability to stimulate lactogenesis, maternal behavior, growth and development, osmoregulation, and epithelial ion transport has been reported in many vertebrates. In our present study, we have targeted the zebrafish prl locus via transcription activator-like effector nucleases (TALENs). Two independent targeted mutant lines with premature termination of the putative sequence of PRL peptides were generated. All prl-deficient zebrafish progeny died at 6-16 days post-fertilization stage (dpf) in egg water. However, the prl-deficient larvae thrived and survived through adulthood in brackish water (5175 mg/L ocean salts), without obvious defects in somatic growth or reproduction. When raised in egg water, the expression levels of certain key Na(+)/Cl(-) cotransporters in the gills and Na(+)/K(+)-ATPase subunits, Na(+)/H(+) exchangers and Na(+)/Cl(-) transporters in the pronephros of prl-deficient larvae were down-regulated at 5 dpf, which caused Na(+)/K(+)/Cl(-) uptake defects in the mutant fish at 6 dpf. Our present results demonstrate that the primary function of zebrafish prl is osmoregulation via governing the uptake and homeostasis of Na(+), K(+) and Cl(-). Our study provides valuable evidence to understand the mechanisms of PRL function better through both phylogenetic and physiological perspectives.
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http://dx.doi.org/10.1038/srep18597DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4698586PMC
January 2016

Depletion of suppressor of cytokine signaling-1a causes hepatic steatosis and insulin resistance in zebrafish.

Am J Physiol Endocrinol Metab 2015 May 10;308(10):E849-59. Epub 2015 Mar 10.

Key Laboratory of Aquatic Biodiversity and Conservation of the Chinese Academy of Sciences, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, Hubei, China; and

Suppressor of cytokine signaling-1a (SOCS1a) is a member of the suppressor of cytokine signaling family, a group of related molecules that mediate the negative regulation of the JAK-STAT pathway. Here, we depleted SOCS1a using the transcription activator-like (TAL) effector nuclease (TALEN) technique to understand its physiological roles in zebrafish. Although elevated levels of JAK-STAT5 activation and erythropoiesis have been observed in socs1a-deficient zebrafish, these animals exhibited normal growth during the early stages. Socs1a-deficient zebrafish began to grow slowly with certain mortalities after 20 days postfertilization (dpf), whereas the heterozygous socs1a-deficient zebrafish exhibited enhanced somatic growth. Decreased adiposity, hepatic steatosis, and insulin resistance were observed in our socs1a-deficient adult zebrafish, which is similar to the lipodystrophy phenotypes observed in mammals. Comparative transcriptomic analyses revealed elevated levels of gluconeogenesis, lipolysis, and hypoxia-inducible response and decreased activities of lipogenesis and glycolysis in the hepatocytes of socs1a-deflicient adult zebrafish. Evident mitochondrial dysfunction has also been observed in hepatocytes from socs1a-deficient zebrafish. Taken together, our results suggest that the negative regulatory roles of SOCS1a on JAK-STAT5 signaling may be involved in the suppression of the erythropoiesis and growth hormone activities, which was also reflected in the enhanced somatic growth performance observed in the heterozygous socs1a-deficient fish. The differences in the effects caused by SOCS1a depletion on insulin sensitivity, lipid metabolism, and inflammatory responses between zebrafish and mammalian models observed here may reflect differences between the functional mechanisms of SOCS members in terrestrial mammals and aquatic teleosts.
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http://dx.doi.org/10.1152/ajpendo.00540.2014DOI Listing
May 2015
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