Ginsenoside Rg1 alleviates lipopolysaccharide-induced pyroptosis in human periodontal ligament cells via inhibiting Drp1-mediated mitochondrial fission

Archives of Oral Biology, Год журнала: 2023, Номер 147, С. 105632 - 105632

Опубликована: Янв. 28, 2023

Язык: Английский

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Ginsenoside, a potential natural product against liver diseases: a comprehensive review from molecular mechanisms to application

Critical Reviews in Food Science and Nutrition, Год журнала: 2025, Номер unknown, С. 1 - 25

Опубликована: Янв. 15, 2025

Liver disease constitutes a significant cause of global mortality, with its pathogenesis being multifaceted. Identifying effective pharmacological and preventive strategies is imperative for liver protection. Ginsenosides, the major bioactive compounds found in ginseng, exhibit multiple activities including protection against liver-related diseases by mitigating fat accumulation inflammation, preventing hepatic fibrosis, exerting anti-hepatocarcinogenic effects. However, comprehensive overview elucidating regulatory pathways associated ginsenosides remains elusive. This review aims to consolidate molecular mechanisms through which different ameliorate distinct diseases, alongside pathogenic factors underlying ailments. Notably, Rb1 Rg1 demonstrate significantly treating fatty liver, hepatitis, CK Rh2 potent anti-hepatocellular carcinogenic Their these effects primarily involve modulation AMPK, NF-κB, TGF-β, NFR2, JNK, other pathways, thereby attenuating accumulation, inhibition stellate cell activation, promoting apoptosis hepatocellular carcinoma cells. Furthermore, it provides insights into safety profile current applications ginsenosides, facilitating their clinical development. Consequently, present promising prospects management, underscoring potential as valuable therapeutic agents this context.

Язык: Английский

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Protective role of ginsenoside Rg1 in the dynamic progression of liver injury to fibrosis: a preclinical meta-analysis

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Янв. 28, 2025

Background The pathological progression from liver injury to fibrosis is a hallmark of disease, with no effective strategies halt this transition. Ginsenoside Rg1 has demonstrated range hepatoprotective properties; however, systematic preclinical evidence supporting its therapeutic potential for and remains limited. Purpose. This study evaluated the efficacy underlying mechanisms ginsenoside in animal models fibrosis, providing basis future clinical investigation. Methods A review was conducted on studies published PubMed, Web Science, Embase databases up 1 August 2024, adhereing rigorous quality standards. methodological assessed using SYRCLE’s risk bias tool. Meta-analysis subgroup analysis were performed Revman 5.4 software, while publication through funnel plots Egger’s test STATA 15.0 software. Additionally, time-dose interval curve utilized assess dose-response relationship identify dose treating fibrosis. Results Twenty-four trials involving 423 animals included. findings indicated that significantly improved function markers (ALT AST), reduced indicators associated lowered fibrosis-related (α-SMA, HYP, PCIII). Furthermore, it exhibited beneficial effects mechanistic inflammation, oxidative stress, apoptosis, compared control group ( P < 0.05). Time-dose revealed between 4 800 mg/kg/d. Conclusion at 4–800 mg/kg/d mitigates via anti-inflammatory, antioxidative, anti-apoptotic pathways. Systematic Review Registration https://www.crd.york.ac.uk/PROSPERO/ , identifier CRD 42024557878.

Язык: Английский

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Breaking the Feedback Loop of β-Cell Failure: Insight into the Pancreatic β-Cell’s ER-Mitochondria Redox Balance

Cells, Год журнала: 2025, Номер 14(6), С. 399 - 399

Опубликована: Март 8, 2025

Pancreatic β-cells rely on a delicate balance between the endoplasmic reticulum (ER) and mitochondria to maintain sufficient insulin stores for regulation of whole animal glucose homeostasis. The ER supports proinsulin maturation through oxidative protein folding, while supply energy redox buffering that proteostasis. In development Type 2 diabetes (T2D), progressive decline β-cell function is closely linked disruptions in ER-mitochondrial communication. Mitochondrial dysfunction well-established driver failure, whereas downstream consequences homeostasis have only recently emerged. This interdependence functions suggests an imbalance both cause consequence metabolic dysfunction. this review, we discuss regulatory mechanisms control requirements mitochondrial function. addition, describe how imbalances may trigger vicious feed forward cycle accelerates T2D onset.

Язык: Английский

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Ginsenoside Rg1 attenuates the NASH phenotype by regulating the miR-375-3p/ATG2B/PTEN-AKT axis to mediate autophagy and pyroptosis

Lipids in Health and Disease, Год журнала: 2023, Номер 22(1)

Опубликована: Фев. 10, 2023

Nonalcoholic steatohepatitis (NASH) is one of the most frequent liver diseases at present, and there no radical treatment. The consequences a variety ginsenoside compounds on this situation have before been reported, however, specific effect monomeric Rg1 (Rg1) its associated underlying molecular mechanism stay unknown.In vitro, cell models were constructed by exposing free fatty acids (FFAs) to HepG2 cells. A methionine choline deficiency (MCD)-induced NASH mouse model was also established over 5-6 weeks traditional Chinese medicine monomer. These treated with analyzed qRT-PCR, Western Blot, sequencing, Oil red O staining, immunofluorescence, enzyme activity, HE ELISA, double luciferase reporter assay, immunohistochemistry.Overexpression ATG2B, an autophagy-related protein, attenuated lipid droplet accumulation reduces ALT, AST, inflammatory cytokines, hydrogen peroxide, pyroptosis in cellular increased levels ATP autophagy. binding sites miR-375-3p ATG2B verified bioinformatic prediction dual-luciferase gene. Knockdown promoted autophagy inhibited pyroptosis. knockdown substantially impact NASH. appears regulate occurrence development inflammation through vitro vivo, regulated PTEN-AKT pathway.This study showed that participates miR-375-3p/ATG2B/PTEN-AKT pathway, thereby alleviating NASH, for reason revealing as candidate drug

Язык: Английский

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Functional Food Chemical Ingredient Strategies for Non-alcoholic Fatty Liver Disease (NAFLD) and Hepatic Fibrosis: Chemical Properties, Health Benefits, Action, and Application

Current Nutrition Reports, Год журнала: 2024, Номер 13(1), С. 1 - 14

Опубликована: Янв. 3, 2024

Язык: Английский

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Aging, ROS, and cellular senescence: a trilogy in the progression of liver fibrosis

Biogerontology, Год журнала: 2024, Номер 26(1)

Опубликована: Ноя. 15, 2024

Язык: Английский

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Ginsenoside Rg1 Mitigates Porcine Intestinal Tight Junction Disruptions Induced by LPS through the p38 MAPK/NLRP3 Inflammasome Pathway

Toxics, Год журнала: 2022, Номер 10(6), С. 285 - 285

Опубликована: Май 27, 2022

Inflammation leads to porcine tight junction disruption of small intestinal epithelial cells, resulting in dysfunction. Herein, we established lipopolysaccharide (LPS)-induced in-vivo and in-vitro inflammatory models. The results revealed that LPS induced IPEC-J2 cells by downregulating tight-junction-related protein zonula occludens-1 (ZO-1), occludin claudin-1 expression, while ginsenoside Rg1 rescued such inhibition abrogated the upregulated expression phosphorylation p38 MAPK. MAPK inhibitor (SB203580) showed a similar effect with attenuated LPS-induced ZO-1, which is consistent reduced NLRP3 inflammasome IL-1β. Furthermore, specific inhibitors IL-1β result increased protein, demonstrating signaling was associated suppression disruption. Besides, treatment decreased through signaling, caused abnormal morphological changes murine ileum. Meanwhile, partially alleviated In summary, these findings characterized novel mechanism alleviates inhibiting MAPK-mediated pathway.

Язык: Английский

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Saponins as potential novel NLRP3 inflammasome inhibitors for inflammatory disorders

Archives of Pharmacal Research, Год журнала: 2024, Номер 47(10-11), С. 757 - 792

Опубликована: Ноя. 1, 2024

Язык: Английский

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Insight into the regulation of NLRP3 inflammasome activation by mitochondria in liver injury and the protective role of natural products

Biomedicine & Pharmacotherapy, Год журнала: 2022, Номер 156, С. 113968 - 113968

Опубликована: Ноя. 4, 2022

Due to high mortality rates and poor prognosis, liver injury remains one of the leading causes worldwide. Amounting evidence suggested that activation nucleotide-binding oligomerization domain (NOD)-like receptor containing pyrin 3 (NLRP3) inflammasome, which promotes pro-interleukin-1β (pro-IL-1β) pro-interleukin-18 (pro-IL-18) cleavage maturation play a vital role in occurrence development disease. Mitochondrial dysfunction is common co-occurring event injury. Abnormal mitochondrial function has also been shown be closely related NLRP3 inflammasome activation. Currently, natural products have attracted attention researchers as potential therapeutic agents for disease due their less toxicity multi-targeting advantages. A number discovered prevent treat by modulating inflammasome. In this review, we highlight mechanisms involved regulation mitochondria during target processes or Our paper may shed insight into novel viewpoint prevention treatment based on

Язык: Английский

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