Gypenosides reverses depressive behavior via inhibiting hippocampal neuroinflammation

Dong, Shuqi; Zhang, Qiuping; Zhu, Ji-Xiao; Chen, Min; Li, Cheng-Fu; Liu, Qing; Geng, Di; Yi, Long

doi:10.1016/j.biopha.2018.07.040

Cited by 44 publications

(24 citation statements)

References 42 publications

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“…One of the IkB kinase subunits, IKKB, encoded by the IKBKB gene, is known to regulate NF-kB activity [ 43 ]. Studies have suggested that chronic unpredictable mild stress (CUMS) induces an increase of IKKB protein levels in the hippocampus [ 69 ]; however, our present findings indicate that CMS reduced IKBKB mRNA levels in the hippocampus, as well as in the amygdala and midbrain. In addition, in contrast to the brain, CMS resulted in increased IKBKB mRNA expression in PMBCs, which was decreased by venlafaxine treatment.…”

Section: Discussioncontrasting

confidence: 97%

“…In addition, in contrast to the brain, CMS resulted in increased IKBKB mRNA expression in PMBCs, which was decreased by venlafaxine treatment. Therefore, it is possible that inhibition of IKKB- NF-kB signaling pathways may exert an antidepressant-like effect and silence the neuroinflammation [ 69 , 70 ]. As the activation of NF-kB signaling promotes the release of proinflammatory cytokines, increased mRNA expression of IKBKB in PMBCs, which acts as a regulatory factor for NF-kB, could contribute to the activation of inflammatory pathways in blood cells; however, this effect is not reflected in the brain.…”

Section: Discussionmentioning

confidence: 99%

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Chronic Mild Stress and Venlafaxine Treatment Were Associated with Altered Expression Level and Methylation Status of New Candidate Inflammatory Genes in PBMCs and Brain Structures of Wistar Rats

Białek

Czarny

Wigner

et al. 2021

Genes

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Preclinical studies conducted to date suggest that depression could be elicited by the elevated expression of proinflammatory molecules: these play a key role in the mediation of neurochemical, neuroendocrine and behavioral changes. Thus, this study investigates the effect of chronic mild stress (CMS) and administration of venlafaxine (SSRI) on the expression and methylation status of new target inflammatory genes: TGFA, TGFB, IRF1, PTGS2 and IKBKB, in peripheral blood mononuclear cells (PMBCs) and in selected brain structures of rats. Adult male Wistar rats were subjected to the CMS and further divided into matched subgroups to receive vehicle or venlafaxine. TaqMan gene expression assay and methylation-sensitive high-resolution melting (MS-HRM) were used to evaluate the expression of the genes and the methylation status of their promoters, respectively. Our results indicate that both CMS and chronic treatment with venlafaxine were associated with changes in expression of the studied genes and their promoter methylation status in PMBCs and the brain. Moreover, the effect of antidepressant administration clearly differed between brain structures. Summarizing, our results confirm at least a partial association between TGFA, TGFB, IRF1, PTGS2 and IKBKB and depressive disorders.

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Section: Discussioncontrasting

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Chronic Mild Stress and Venlafaxine Treatment Were Associated with Altered Expression Level and Methylation Status of New Candidate Inflammatory Genes in PBMCs and Brain Structures of Wistar Rats

Białek

Czarny

Wigner

et al. 2021

Genes

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“…Mice were randomly divided into PBS, LPS, GPs and GPs + LPS groups (n = 3). Mice received intratracheal administration of PBS (50ul), intratracheal administration of LPS (5 mg/kg, in 50ul PBS), intraperitoneal injection of GPs (100 mg/kg, in 300ul PBS), 21 or intraperitoneal injection of GPs + intratracheal administration of LPS, respectively. A brief description of the experimental process is described in Figure 2A.…”

Section: Gps Alleviated Lung Injury and Improved The Survival Ratio Of Ali Micementioning

confidence: 99%

“…In spite of positive results of potential therapeutic effects of GPs in ALI in the study, there also existed some limitations. The dosage of intraperitoneal GPs of 100 mg/kg in vivo was applied as previously described, 21 maybe the dosage was not optimal. In order to be consistent with in vivo experiments, the HPMEC and MLE-12 were stimulated for 8h, while some experiments detected p-p65 expression in LPSstimulated cells only after 30 min.…”

Section: Dovepressmentioning

confidence: 99%

Gypenosides Inhibit Inflammatory Response and Apoptosis of Endothelial and Epithelial Cells in LPS-Induced ALI: A Study Based on Bioinformatic Analysis and in vivo/vitro Experiments

Zhu

Yuan

et al. 2021

DDDT

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Introduction: Severe inflammatory response leads to poor prognosis of acute lung injury (ALI), the role of gypenosides (GPs) on ALI is not fully clear. The study aimed at investigating the effects of GPs on ALI. Methods: We firstly established LPS-induced ALI mice model. Then, we tested whether GPs contributed to alleviate inflammatory response and lung injury of ALI in vivo. In order to identify specific mechanisms of the phenomenon, we conducted a bioinformatic analysis of LPS-induced ALI mice based on GEO database to identify hub differentially expressed genes (DEGs). PPI network of the DEGs was used to find hub-genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were conducted based on the DAVID database to identify which pathways the genes enriched. Then, we tested whether GPs inhibited lung injury and inflammatory response via the enriched pathways. We also tested whether GPs inhibited the apoptosis of endothelial and epithelial cells secondary to severe inflammation. Results: We found GPs significantly alleviated lung injury and improved the survival rate of LPS-induced ALI mice in vivo. Bioinformatic analysis identified 20 hub-genes from DEGs, they were mainly enriched in NF-κB and TNF-α pathways. GPs could reduce the lung injury and inflammatory response via inhibiting NF-κB and TNF-α pathways in vivo. Our results indicated that GPs also inhibited inflammatory response of epithelial and endothelial cells via NF-κB and TNF-α pathways in vitro. Severe inflammatory response could also lead to apoptosis of endothelial and epithelial cells. Our results indicated that GPs effectively inhibited the apoptosis of endothelial and epithelial cells. Conclusion:Our study suggested GPs contributed to alleviated lung injury in vivo and inhibited inflammation and apoptosis of endothelial and epithelial cells in vitro, providing novel strategies for the prevention and therapy for ALI.

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“…Gynostemma pentaphyllum is the root or whole plant of Gynura Gynostemma [4]. Some studies have identified that Gynostemma pentaphyllum has functions in lowering blood fat, preventing arteriosclerosis, resisting oxidation, lowering blood sugar, and regulating immunity [5][6][7][8][9]. Gypenosides is an extraction product of Gynostemma pentaphyllum, which has multiple pharmacological activities [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Gypenoside Inhibits Endothelial Cell Apoptosis in Atherosclerosis by Modulating Mitochondria through PI3K/Akt/Bad Pathway

Song

Cao

et al. 2020

BioMed Research International

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Atherosclerosis remains the most common cause of deaths worldwide. Endothelial cell apoptosis is an important process in the progress of atherosclerosis, as it can cause the endothelium to lose their capability in regulating the lipid homeostasis, inflammation, and immunity. Endothelial cell injury can disrupt the integrity and barrier function of an endothelium and facilitate lipid deposition, leading to atherogenesis. Chinese medicine techniques for preventing and treating atherosclerosis are gaining attention, especially natural products. In this study, we demonstrated that gypenoside could decrease the levels of serum lipid, alleviate the formation of atherosclerotic plaque, and lessen aortic intima thickening. Gypenoside potentially activates the PI3K/Akt/Bad signal pathway to modulate the apoptosis-related protein expression in the aorta. Moreover, gypenoside downregulated mitochondrial fission and fusion proteins, mitochondrial energy-related proteins in the mouse aorta. In conclusion, this study demonstrated a new function of gypenoside in endothelial apoptosis and suggested a therapeutic potential of gypenoside in atherosclerosis associated with apoptosis by modulating mitochondrial function through the PI3K/Akt/Bad pathway.

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Gypenosides reverses depressive behavior via inhibiting hippocampal neuroinflammation

Cited by 44 publications

References 42 publications

Chronic Mild Stress and Venlafaxine Treatment Were Associated with Altered Expression Level and Methylation Status of New Candidate Inflammatory Genes in PBMCs and Brain Structures of Wistar Rats

Chronic Mild Stress and Venlafaxine Treatment Were Associated with Altered Expression Level and Methylation Status of New Candidate Inflammatory Genes in PBMCs and Brain Structures of Wistar Rats

Gypenosides Inhibit Inflammatory Response and Apoptosis of Endothelial and Epithelial Cells in LPS-Induced ALI: A Study Based on Bioinformatic Analysis and in vivo/vitro Experiments

Gypenoside Inhibits Endothelial Cell Apoptosis in Atherosclerosis by Modulating Mitochondria through PI3K/Akt/Bad Pathway

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