Ginsenoside Rg1 protects against sepsis-associated encephalopathy through beclin 1–independent autophagy in mice

Li, Yinjiao; Wang, Fang; Luo, Yan

doi:10.1016/j.jss.2016.08.080

Cited by 54 publications

(37 citation statements)

References 31 publications

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“…It is well-known that KRGE contains several ginsenosides (Rg1, Rg3, Rh2, Rb1, and Re), which are known to regulate autophagy. [16][17][18][19][20] Further studies will be needed to define the role of each ginsenoside in Tac-induced DM. Second, we expected the marked effect of KRGE on Tacinduced DM but it did not.…”

Section: Discussionmentioning

confidence: 99%

Ginseng extract reduces tacrolimus-induced oxidative stress by modulating autophagy in pancreatic beta cells

Lim

Jin

Luo

et al. 2017

Laboratory Investigation

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We previously reported that long-term treatment with a calcineurin inhibitor impairs autophagy process in pancreatic beta cells. This study investigated the effect of Korean red ginseng extract (KRGE) on autophagy modulated by oxidative stress. In mice with tacrolimus (Tac)-induced diabetes mellitus, KRGE alleviated islet dysfunction and decreased oxidative stress and autophagic vacuoles. In vitro, KRGE decreased autophagosome formation and attenuated lysosomal degradation, accompanied by improved beta cell viability and insulin secretion. Addition of 3-methyladenine (3-MA), an inhibitor of autophagosomes, to KRGE further improved cell viability and insulin secretion, and bafilomycin A (BA), an inhibitor of lysosomal function, reduced the effects of KRGE. At the subcellular level, Tac caused mitochondrial dysfunction (impaired mitochondrial oxygen consumption, ATP production, and increased reactive oxygen species production). But KRGE improved these parameters. The effect of KRGE on mitochondrial function enhanced by 3-MA but decreased by BA, suggesting a causal relationship between KRGE effect and autophagy modulation in Tac-induced mitochondrial dysfunction. These findings indicate that KRGE modulates autophagy favorably by reducing Tac-induced oxidative stress, and this effect is closely associated with improvement of mitochondrial function.

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Section: Discussionmentioning

confidence: 99%

Ginseng extract reduces tacrolimus-induced oxidative stress by modulating autophagy in pancreatic beta cells

Lim

Jin

Luo

et al. 2017

Laboratory Investigation

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“…Ginseng has been used in traditional Chinese medicine formulations for more than 2,000 years and has shown antitransdifferentiation, antioxidant, antiapoptotic, and autophagic effects [14][15][16]. e pharmacological effects of ginseng are mainly attributed to the ginsenosides, primarily the ginsenoside Rg1.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg1 Alleviates Podocyte EMT Passage by Regulating AKT/GSK3 β/β‐Catenin Pathway by Restoring Autophagic Activity

Shi

Gao

Wang

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Background. Diabetic nephropathy (DN), a complication of diabetes, is the result of high glucose-induced pathological changes in podocytes, such as epithelial-mesenchymal transition (EMT). Autophagy is an important mechanism of podocyte repair. Ginsenoside Rg1, the active ingredient of ginseng extract, has antifibrotic and proautophagic effects. Therefore, we hypothesized that ginsenoside Rg1 can reverse podocyte EMT via autophagy and alleviate DN. Aim. This study aimed to investigate the effect of ginsenoside Rg1 on DN rats and high glucose-induced podocyte EMT by regulating the AKT/GSK3β/β-catenin pathway by restoring autophagy activity. Methods. Diabetic rats induced by STZ injection were treated with 50 mg/kg ginsenoside Rg1 for 8 weeks, and the renal functional, metabolic, and histopathological indices were evaluated. DN was simulated in vitro by exposing podocytes to high glucose levels and treated with ginsenoside Rg1. The expression of EMT and autophagy-related markers was analyzed in vivo and in vitro by immunofluorescence, western blotting, and real-time PCR. Results. Ginsenoside Rg1 significantly alleviated renal fibrosis and podocyte EMT in diabetic rats, and podocytes exposed to high glucose levels, which was abolished by the autophagy inhibitor 3-MA. Furthermore, ginsenoside Rg1 regulated the AKT/GSK3 β/β-catenin pathway by restoring autophagic activity. Conclusion. Ginsenoside Rg1 alleviated podocyte EMT by enhancing AKT/GSK3β/β-catenin pathway-mediated autophagy, indicating its therapeutic potential for DN and other glomerular diseases.

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“…Ginsenoside Rg1 could ameliorate sepsis-associated encephalopathy through regulating cerebral in ammation and apoptosis. [56] Ginsenoside Rg3 could improve mitochondrial dysfunction by regulating autophagy in mitochondria via activating the AMPK signal pathway, thus protecting organ injuries caused by sepsis [57].…”

Section: Discussionmentioning

confidence: 99%

YiQiFuMai Lyophilized Injection Attenuates Sepsis-Induced Acute Lung Injury via TLR4/Src/VE-cadherin/p120-catenin Signaling Pathway

Pan¹,

Xue²,

Zhou³

et al. 2020

Preprint

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Background: Sepsis is a severe disorder leading to a clinically critical syndrome of multiple organ dysfunction syndrome. Most patients with sepsis will be associated with acute lung injury (ALI), which is an independent risk factors of organ failure and death in patients with sepsis at the same time. YiQiFuMai Lyophilized Injection (YQFM) is a modern traditional Chinese prescription preparation, which could ameliorate ALI induced by lipopolysaccharide (LPS) or fine particulate matter. The current study aimed to investigate the effect of YQFM on sepsis-induced ALI and the underlying mechanism.Methods: Male C57BL/6J mice were treated with cecal ligation and puncture (CLP) after tail intravenous injected with YQFM (1, 2 and 4 g/kg). The measurements of lung edema, evans blue leakage, myeloperoxidase content, inflammatory cells in bronchoalveolar lavage fluid, histopathological assay and expression of associated proteins were performed at 18 h after CLP.Results: The results illustrated that YQFM inhibited pulmonary edema and inflammatory response, thus ameliorated ALI in sepsis mice. Furthermore, the expression of TLR4 and phosphorylated Src was down-regulated, and the expression of p120-catenin and VE-cadherin was restored by YQFM administration.Conclusion: Our study suggested the therapeutic potential of YQFM on treating sepsis-induced ALI via regulating TLR4/Src/VE-cadherin/p120-catenin signaling pathway.

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Ginsenoside Rg1 protects against sepsis-associated encephalopathy through beclin 1–independent autophagy in mice

Cited by 54 publications

References 31 publications

Ginseng extract reduces tacrolimus-induced oxidative stress by modulating autophagy in pancreatic beta cells

Ginseng extract reduces tacrolimus-induced oxidative stress by modulating autophagy in pancreatic beta cells

Ginsenoside Rg1 Alleviates Podocyte EMT Passage by Regulating AKT/GSK3 β/β‐Catenin Pathway by Restoring Autophagic Activity

YiQiFuMai Lyophilized Injection Attenuates Sepsis-Induced Acute Lung Injury via TLR4/Src/VE-cadherin/p120-catenin Signaling Pathway

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