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Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway
Conclusion In conclusion, the present study demonstrated that autophagy was involved in relieving the effects of TSF against NAFLD, which were mediated by the AMPK/SIRT1 pathway (Figure 7D). These findings may improve our current understanding of the role of TSF in treating hepatic steatosis and provide an experimental basis for the clinical application of TSF in NAFLD and its related metabolic syndrome. Ethics Statement This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Ethics Co...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

Suppression of Rho-kinase 1 is responsible for insulin regulation of the AMPK/SREBP-1c pathway in skeletal muscle cells exposed to palmitate
ConclusionsOur study indicated that insulin reduced lipotoxicity via ROCK1 and then improved AMPK/SREBP-1c signaling in skeletal muscle under PA-induced insulin resistance.
Source: Acta Diabetologica - March 6, 2017 Category: Endocrinology Source Type: research

Metformin Improves the Senescence of Renal Tubular Epithelial Cells in a High-Glucose State Through E2F1
In this study, we explored whether metformin improves a high-glucose-induced senescence and fibrosis of renal tubular epithelial cells through cell cycle-related protein E2F1. In the in vivo experiments, the recombinant adeno-associated virus (AAV-shE2F1) knockdown E2F1 gene was injected into the tail vein of 16-weeks-old db/db mice for 8 weeks. The 16-week-old db/db mice were administered metformin (260 mg/kg/d) continuously for 8 weeks. The normal control group (NC) and diabetic model group (DM) were set up simultaneously. Mice renal tubular epithelial cells (mRTECs) were cultured in vitro. The cells were randomly div...
Source: Frontiers in Pharmacology - June 23, 2022 Category: Drugs & Pharmacology Source Type: research

Metformin-mediated downregulation of p38 mitogen-activated protein kinase-dependent excision repair cross-complementing 1 decreases DNA repair capacity and sensitizes human lung cancer cells to paclitaxel.
Abstract Metformin, an extensively used and well-tolerated drug for treating individuals with type 2 diabetes, has recently gained significant attention as an anticancer drug. On the other hand, paclitaxel (Taxol) is a new antineoplastic drug that has shown promise in the treatment of non-small cell lung cancer (NSCLC). High expression levels of excision repair cross-complementary 1 (ERCC1) in cancers have been positively associated with the DNA repair capacity and a poor prognosis in NSCLC patients treated with platinum-containing chemotherapy. In this current study, paclitaxel was found to increase phosphorylati...
Source: Biochemical Pharmacology - December 7, 2012 Category: Drugs & Pharmacology Authors: Tseng SC, Huang YC, Chen HJ, Chiu HC, Huang YJ, Wo TY, Weng SH, Lin YW Tags: Biochem Pharmacol Source Type: research

Involvement of the AMPK-PTEN pathway in insulin resistance induced by high glucose in cultured rat podocytes.
Abstract As part of the filtration barrier, podocytes play an important role in the development of diabetic nephropathy. Disturbances in insulin signaling accompanied by insulin resistance can lead to various intracellular events. We hypothesized that high glucose concentrations would lead to disturbances in interactions between AMPK and PTEN proteins in podocytes. Experiments were performed in primary rat podocytes cultured with normal (5.6mM) or high (30mM) glucose concentrations for 5 d. Immunodetection methods were used to detect AMPK, PTEN, insulin receptor, and Akt proteins, and their phosphorylated forms. I...
Source: The International Journal of Biochemistry and Cell Biology - April 15, 2014 Category: Biochemistry Authors: Rogacka D, Piwkowska A, Audzeyenka I, Angielski S, Jankowski M Tags: Int J Biochem Cell Biol Source Type: research

Metformin inhibits growth of human non-small cell lung cancer cells via liver kinase B-1-independent activation of adenosine monophosphate-activated protein kinase.
Authors: Guo Q, Liu Z, Jiang L, Liu M, Ma J, Yang C, Han L, Nan K, Liang X Abstract Metformin, the most widely administered oral anti‑diabetic therapeutic agent, exerts its glucose-lowering effect predominantly via liver kinase B1 (LKB1)-dependent activation of adenosine monophosphate-activated protein kinase (AMPK). Accumulating evidence has demonstrated that metformin possesses potential antitumor effects. However, whether the antitumor effect of metformin is via the LKB1/AMPK signaling pathway remains to be determined. In the current study, the effects of metformin on proliferation, cell cycle progression, and...
Source: Molecular Medicine Reports - February 9, 2016 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

The roles of tricellular tight junction protein lipolysis-stimulated lipoprotein receptor in malignancy of human endometrial cancer cells.
Authors: Shimada H, Satohisa S, Kohno T, Takahashi S, Hatakeyama T, Konno T, Tsujiwaki M, Saito T, Kojima T Abstract Lipolysis-stimulated lipoprotein receptor (LSR) has been identified as a novel molecular constituent of tricellular contacts that have a barrier function for the cellular sheet. LSR recruits tricellulin (TRIC), which is the first molecular component of tricellular tight junctions. Knockdown of LSR increases cell motility and invasion of certain cancer cells. However, the behavior and the roles of LSR in endometrial cancer remain unknown. In the present study, we investigated the behavior and roles of...
Source: Oncotarget - April 3, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Metformin Enhances Autophagy and Normalizes Mitochondrial Function to Alleviate Aging-Associated Inflammation.
Abstract Age is a non-modifiable risk factor for the inflammation that underlies age-associated diseases; thus, anti-inflammaging drugs hold promise for increasing health span. Cytokine profiling and bioinformatic analyses showed that Th17 cytokine production differentiates CD4+ T cells from lean, normoglycemic older and younger subjects, and mimics a diabetes-associated Th17 profile. T cells from older compared to younger subjects also had defects in autophagy and mitochondrial bioenergetics that associate with redox imbalance. Metformin ameliorated the Th17 inflammaging profile by increasing autophagy and impr...
Source: Cell Metabolism - May 4, 2020 Category: Cytology Authors: Bharath LP, Agrawal M, McCambridge G, Nicholas DA, Hasturk H, Liu J, Jiang K, Liu R, Guo Z, Deeney J, Apovian CM, Snyder-Cappione J, Hawk GS, Fleeman RM, Pihl RMF, Thompson K, Belkina AC, Cui L, Proctor EA, Kern PA, Nikolajczyk BS Tags: Cell Metab Source Type: research

Metformin Induces Cytotoxicity by Down‐Regulating Thymidine Phosphorylase and ERCC1 Expression in Non‐Small Cell Lung Cancer Cells
In conclusion, metformin induces cytotoxicity by down‐regulating TP and ERCC1 expression in NSCLC cells.
Source: Basic and Clinical Pharmacology and Toxicology - January 31, 2013 Category: Drugs & Pharmacology Authors: Jen‐Chung Ko, Yu‐Ching Huang, Huang‐Jen Chen, Sheng‐Chieh Tseng, Hsien‐Chun Chiu, Ting‐Yu Wo, Yi‐Jhen Huang, Shao‐Hsing Weng, Robin Y.Y. Chiou, Yun‐Wei Lin Tags: Original Article Source Type: research

Metformin Enhances Cisplatin Cytotoxicity by Suppressing Stat3 Activity Independently of the LKB1-AMPK Pathway.
This study demonstrated a correlation between Stat3 phosphorylation and cisplatin cytotoxicity using AS2 (PC14PE6/AS2)-derived cell lines (AS2/S3C) that contained constitutively active Stat3 plasmids as a model. A Stat3 inhibitor (JSI-124) enhanced the cisplatin sensitivity in AS2 cells, whereas metformin inhibited Stat3 phosphorylation and enhanced cisplatin cytotoxicity. By contrast, another AMPK activator (AICAR) failed to produce these effects. LKB1-AMPK silencing by siRNA or mTOR inhibition by rapamycin or pp242 did not alter the effect of metformin on Stat3 activity suppression, suggesting that metformin can modulate...
Source: American Journal of Respiratory Cell and Molecular Biology - March 22, 2013 Category: Molecular Biology Authors: Lin CC, Yeh HH, Huang WL, Yan JJ, Lai WW, Su WP, Chen HH, Su WC Tags: Am J Respir Cell Mol Biol Source Type: research

Inhibition of p38 MAPK-dependent MutS homologue-2 (MSH2) expression by metformin enhances gefitinib-induced cytotoxicity in human squamous lung cancer cells
Conclusion: Together, down-regulation of MSH2 expression can be a possible strategy to enhance the sensitivity of gefitinib to human lung squamous cancer cells.
Source: Lung Cancer - October 17, 2013 Category: Cancer & Oncology Authors: Jen-Chung Ko, Hsien-Chun Chiu, Ting-Yu Wo, Yi-Jhen Huang, Sheng-Chieh Tseng, Yu-Ching Huang, Huang-Jen Chen, Jhan-Jhang Syu, Chien-Yu Chen, Yun-Ting Jian, Yi-Jun Jian, Yun-Wei Lin Tags: Carcinogenesis and molecular biology Source Type: research

Metformin anti-tumor effect via disruption of the MID1 translational regulator complex and AR downregulation in prostate cancer cells
Conclusions: Findings reported herein uncover a mechanism for the anti-tumor activity of metformin in prostate cancer, which is independent of its anti-diabetic effects. These data provide a rationale for the use of metformin in the treatment of hormone naive and castration-resistant prostate cancer and suggest AR is an important indirect target of metformin.
Source: BMC Cancer - January 31, 2014 Category: Cancer & Oncology Authors: Ummuhan DemirAndrea KoehlerRainer SchneiderSusann SchweigerHelmut Klocker Source Type: research

Small Heterodimer Partner Blocks Cardiac Hypertrophy by Interfering with GATA6 Signaling.
Conclusions: These results establish SHP as a novel anti-hypertrophic regulator that acts by interfering with GATA6 signaling. SHP may participate in the metformin-induced anti-hypertrophic response. PMID: 25015078 [PubMed - as supplied by publisher]
Source: Circulation Research - July 11, 2014 Category: Cardiology Authors: Nam YS, Kim Y, Joung H, Kwon DH, Choe N, Min HK, Kim Y, Kim HS, Kim DK, Cho YK, Kim YH, Nam KI, Choi HC, Park DH, Suk K, Lee IK, Ahn Y, Lee CH, Choi HS, Eom GH, Kook H Tags: Circ Res Source Type: research

Metformin promotes irisin release from murine skeletal muscle independently of AMPK activation
ConclusionMetformin promotes irisin release from murine skeletal muscle into blood, independently of AMPK pathway activation. Our results suggest that stimulation of irisin may be a novel molecular mechanism of metformin which is widely used for treatment of metabolic disorders.This article is protected by copyright. All rights reserved.
Source: Acta Physiologica - November 11, 2014 Category: Physiology Authors: Dong‐Jie Li, Fang Huang, Wen‐Jie Lu, Guo‐Jun Jiang, Ya‐ping Deng, Fu‐Ming Shen Tags: Regular Paper Source Type: research

Metformin promotes irisin release from murine skeletal muscle independently of AMP‐activated protein kinase activation
ConclusionMetformin promotes irisin release from murine skeletal muscle into blood, independently of AMPK pathway activation. Our results suggest that stimulation of irisin may be a novel molecular mechanism of metformin which is widely used for treatment of metabolic disorders.
Source: Acta Physiologica - November 24, 2014 Category: Physiology Authors: D.‐J. Li, F. Huang, W.‐J. Lu, G.‐J. Jiang, Y.‐P. Deng, F.‐M. Shen Tags: Original Article Source Type: research

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