Publications by authors named "Guoji Zhu"

6 Publications

  • Page 1 of 1

Atorvastatin Relieves Cognitive Disorder After Sepsis Through Reverting Inflammatory Cytokines, Oxidative Stress, and Neuronal Apoptosis in Hippocampus.

Cell Mol Neurobiol 2020 May 6;40(4):521-530. Epub 2019 Nov 6.

Neonate Department, Soochow University Affiliated Children's Hospital, Suzhou, People's Republic of China.

This present research work reports the possible effects and the underlying mechanism of atorvastatin on survival rate and cognitive disorders after sepsis. Sepsis is a life-threatening dysfunction that arises when the body's response to infection causes injury to its own tissues and organs. Diffuse sepsis was induced by cecal ligation and puncture surgery (CLP) in ICR mice. 0.2 mg/kg body weight of atorvastatin was administrated intraperitoneally at 12 h before surgery. The survival of mice was calculated 24 h, 48 h, 72 h, and 96 h after CLP surgery. Two weeks later, open-field test and Morris water maze test were conducted to evaluate the protective effect of atorvastatin. Inflammatory cytokines in plasma, oxidative stress parameters, number of astrocytes, and neuronal cell deaths in the CA3 region of the hippocampus were examined using enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry. The results indicate that pretreatment with atorvastatin can increase survival percentage and improve cognitive function. Atorvastatin reversed all these alterations in parallel with a decrease in circulating levels of cytokines (IL-1β, IL-4, IL-6, and TNF-α) in plasma, inhibited the activities of oxidative stress parameters (lower TBARS levels, ratio of GSH/GSSH, and activities of SOD and CAT), enhanced the activity of citrate synthase in brain, and reduced the number of astrocytes and neuronal cell deaths in CA3 region of hippocampus. Overall, our results indicated that atorvastatin exhibited protective effects on survival rate and cognitive disorders after sepsis by inhibiting the release of inflammatory cytokines, oxidative stress, and neuronal apoptosis in brain tissue.
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http://dx.doi.org/10.1007/s10571-019-00750-zDOI Listing
May 2020

Metformin ameliorates sepsis-induced brain injury by inhibiting apoptosis, oxidative stress and neuroinflammation via the PI3K/Akt signaling pathway.

Oncotarget 2017 Nov 10;8(58):97977-97989. Epub 2017 Aug 10.

Department of Internal Medicine, Soochow University Affiliated Children's Hospital, Suzhou, Jiangsu, P.R. China.

Sepsis-induced brain injuries increase mortality, morbidity, cognitive impairment and lack of effective therapeutic treatment. Previous studies have suggested that metformin provides neuroprotective effects against ischemia, brain trauma and other brain damage, but whether metformin protects a septic brain remains unknown. Thus, the aim of this study is to investigate the possible effects and the mechanism of metformin against septic brain damage using the cecal ligation and puncture (CLP) model. Mice were randomly divided into five groups: the Sham group, CLP group, CLP+ Met group, CLP+ vehicle group and CLP+ Met+ LY group. The survival percentage and brain water content were examined, and the Morris water maze was conducted to determine the protective effect of metformin. Neuronal apoptosis in the cerebral cortex, striatum and hippocampus was examined using TUNEL assay and immunohistochemistry, and western blot was applied to measure the expression of p-Akt. The results indicate that metformin can increase survival percentage, decrease brain edema, preserve the blood-brain barrier (BBB) and improve cognitive function. Metformin also reduced the neuronal apoptosis induced by sepsis and increased the phosphorylation of Akt. However, the protective effect of metformin can be reversed by LY294002, a PI3K inhibitor. In summary, our results demonstrate that metformin can exert a neuroprotective effect by activating the PI3K/Akt signaling pathway.
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http://dx.doi.org/10.18632/oncotarget.20105DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716707PMC
November 2017

Inhibition of TNF-α sepsis of lipopolysaccharide induction using nano cerium oxide system.

Mater Sci Eng C Mater Biol Appl 2017 Aug 23;77:405-410. Epub 2017 Mar 23.

Department of Internal Medicine, Soochow University Affiliated Children's Hospital, Suzhou, Jiangsu 215003, PR China. Electronic address:

Nowadays sepsis was one of the major threatening issues all over the globe which majorly causes death in high rate. To treat sepsis only few reports have been proposed with the help of anti-oxidants. This manuscript stated that the grape is rich in anti-oxidant, with the help of anti-oxidant rich grape extract Cerium oxide nanoparticles (CeO NPs) were synthesized eco-friendly. Further the synthesized CeO NPs subjected for various characterization studies which resulted in 37nm of size with agglomerated spherical shape particles. Further synthesized CeO NPs were subjected in vivo through tail nerves of rats to treat sepsis. CeO NPs stops the release TNF-α and tends to increase the ceria level in liver. Histopathological studies were performed and also reported. The obtained results were statistically significant with ANOVA LSD-Tukey's test were studied and reported in this manuscript.
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http://dx.doi.org/10.1016/j.msec.2017.03.207DOI Listing
August 2017

Expression of NLRC4 in children with septicaemia and mechanisms of NLRC4 in in vitro cytokine secretion.

Mol Med Rep 2016 Jul 12;14(1):509-14. Epub 2016 May 12.

Department of Internal Medicine, Soochow University Affiliated Children's Hospital, Suzhou, Jiangsu 215003, P.R. China.

Septicaemia, a systemic bacterial infection, frequently leads to morbidity and mortality in children. The NOD-like receptor (NLR) family, CARD domain containing 4 (NLRC4) is involved in the control of infections. The aim of the present study was to detect the expression of NLRC4 in the blood samples of children with septicaemia, in addition to investigating the importance of NLRC4 in cytokine production, and the signaling pathways that regulate NLRC4 expression in lipopolysaccharide (LPS)-stimulated macrophages. It was determined that when compared with the control, the mRNA and protein expression levels of NLRC4 were significantly increased in the blood samples of children with septicaemia, as demonstrated by the reverse transcription‑quantitative polymerase chain reaction and western blot analysis. The results from the western blotting indicated that treatment with LPS induced NLRC4 expression in a time‑ and dose‑dependent manner in RAW264.7 cells. A knockdown of NLRC4 by siRNA transfection enhanced the effect of LPS on interleukin (IL)‑1β and IL‑18 production, as determined by enzyme‑linked immunosorbent assay. Inhibitors of extracellular regulated protein kinases, c‑Jun N‑terminal kinases and p38 were used in the present study to block the mitogen‑activated protein kinase (MAPK) signaling pathway, and it was determined that LPS‑induced NLRC4 expression was reversed by the suppression of the MAPK signaling pathway. To the best of our knowledge, this is the first report regarding the expression of NLRC4 in children with septicaemia. Furthermore, a novel molecular mechanism for NLRC4 regulation in LPS‑induced RAW264.7 macrophage cells has been elucidated. The data in the present study supports the hypothesis that LPS activates the MAPK pathway in macrophages, thus resulting in the upregulation of NLRC4; however, NLRC4 inhibits IL‑1β and IL‑18 production, contributing to the anti-inflammatory response.
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http://dx.doi.org/10.3892/mmr.2016.5254DOI Listing
July 2016

Combined use of biomarkers for distinguishing between bacterial and viral etiologies in pediatric lower respiratory tract infections.

Infect Dis (Lond) 2015 May 24;47(5):289-93. Epub 2015 Feb 24.

Department of Internal Medicine, Soochow University Affiliated Children's Hospital , Soochow , China.

Background: In clinical practice it is often troublesome to discriminate bacterial etiologies from viral etiologies in pediatric lower respiratory tract infections (LRTIs). The aim of this study was to develop an accurate analytic method to improve diagnostic determination for bacterial and viral etiologies in pediatric LRTIs.

Methods: A total of 45 children with confirmed bacterial LRTIs and 51 children with viral LRTIs were finally included after assessment of the children visiting the emergency department with a suspected infection and identification of pathogens. C-reactive protein (CRP), procalcitonin (PCT), interleukin-6 (IL-6), CD35, and CD64 were assessed and then the areas under receiver operating characteristic (ROC) curves (AUC) of PCT, IL-6, CD35, and CD64 in combination with CRP were compared to the AUC of CRP alone in all subjects.

Results: The levels of CRP, PCT, IL-6, CD45, and CD64 observed in children with bacterial LRTIs were statistically higher than for viral infections. The AUC of CRP combined with CD53 (0.963, 95% confidence interval (CI) 0.921-1.002) or CD64 (0.952, 95% CI 0.907-0.998) or CD35/CD64 (0.971, 95% CI 0.932-1.004) increased compared with that of the single biomarker.

Conclusions: The combined analysis improved diagnostic accuracy in children with bacterial and viral LRTIs.
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http://dx.doi.org/10.3109/00365548.2014.987163DOI Listing
May 2015

Impaired cytokine production and decreased TLR2-mediated signaling in mouse infant macrophages.

Fetal Pediatr Pathol 2012 Dec 23;31(6):365-73. Epub 2012 Mar 23.

Soochow University Affiliated Children's Hospital, Suzhou, China.

Infants are known to be more susceptible to pathogens. This might be due in part to the impaired function of macrophage. In the present study, we observed that macrophages from infant mice produced decreased levels of TNF-α and IL-6, but increased IL-10 after stimulation with toll-like receptor 2 (TLR2) agonist zymosan. Moreover, zymosan-stimulated activation of mitogen-activated protein kinase (MAPK) p38 and ERK1/2 was significantly reduced in mouse infant macrophages. These effects could be reversed by using MAPK modulators. The findings suggest that the impaired cytokine production and decreased TLR2-mediated signaling in infant macrophages may contribute to the susceptibility of infants to bacterial infection.
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http://dx.doi.org/10.3109/15513815.2012.659401DOI Listing
December 2012
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