Isorhamnetin: A hepatoprotective flavonoid inhibits apoptosis and autophagy via P38/PPAR-α pathway in mice

Lu, Xiya; Liu, Tong; Chen, Kan; Xia, Yujing; Dai, Weiqi; Xu, Shizan; Xu, Ling; Wang, Fan; Wu, Liwei; Li, Jingjing; Li, Sainan; Wang, Wenwen; Yu, Qiang; Jiao, Feng; Fan, Xiaoming; Zhou, Yingqun; Niu, Peiqin; Guo, Chuanyong

doi:10.1016/j.biopha.2018.04.016

Cited by 68 publications

(47 citation statements)

References 42 publications

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“…We also have published some reports on the effects of PPARs in liver diseases. The protective effects of many Chinese herbal medicines, such as quercetin, oleanolic acid, proanthocyanidin B2, epigallocatechin‐3‐gallate, isorhamnetin and genistein, in liver diseases have been confirmed by our studies.…”

Section: Pparγ Agonists From Natural Productssupporting

confidence: 76%

Therapeutic potential of PPARγ natural agonists in liver diseases

Guo

2020

J Cellular Molecular Medi

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Peroxisome proliferator‐activated receptor gamma (PPARγ) is a vital subtype of the PPAR family. The biological functions are complex and diverse. PPARγ plays a significant role in protecting the liver from inflammation, oxidation, fibrosis, fatty liver and tumours. Natural products are a promising pool for drug discovery, and enormous research effort has been invested in exploring the PPARγ‐activating potential of natural products. In this manuscript, we will review the research progress of PPARγ agonists from natural products in recent years and probe into the application potential and prospects of PPARγ natural agonists in the therapy of various liver diseases, including inflammation, hepatic fibrosis, non‐alcoholic fatty liver and liver cancer.

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Section: Pparγ Agonists From Natural Productssupporting

confidence: 76%

Therapeutic potential of PPARγ natural agonists in liver diseases

Guo

2020

J Cellular Molecular Medi

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“…Animal tissues were immersed in 4% paraformaldehyde for at least 24 h, then embedded in paraffin and cut into 3 μm thick sections. The H&E, IHC and TUNEL staining was carried out as described previously [31,32].…”

Section: Subcutaneous Xenograft Tumor Modelmentioning

confidence: 99%

Simvastatin re-sensitizes hepatocellular carcinoma cells to sorafenib by inhibiting HIF-1α/PPAR-γ/PKM2-mediated glycolysis

Jiao

Dai

Mao

et al. 2020

J Exp Clin Cancer Res

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149

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Background: Hepatocellular carcinoma (HCC) is a common primary malignant tumor which usually progresses to an advanced stage because of late diagnosis. Sorafenib (Sora) is a first line medicine for advanced stage HCC; however, it has been faced with enormous resistance. Simvastatin (Sim) is a cholesterol-lowering drug and has been reported to inhibit tumor growth. The present study aims to determine whether Sora and Sim co-treatment can improve Sora resistance in HCC. Methods: The HCC cell line LM3 and an established Sora-resistant LM3 cell line (LM3-SR) were used to study the relationship between Sora resistance and aerobic glycolysis. Cell proliferation, apoptosis and glycolysis levels were analyzed by western blotting, flow cytometry analysis and biomedical tests. A xenograft model was also used to examine the effect of Sim in vivo. Detailed mechanistic studies were also undertaken by the use of activators and inhibitors, and lentivirus transfections.Results: Our results demonstrated that the resistance to Sora was associated with enhanced aerobic glycolysis levels. Furthermore, LM3-SR cells were more sensitive to Sim than LM3 cells, suggesting that combined treatment with both Sora and Sim could enhance the sensitivity of LM3-SR cells to Sora. This finding may be due to the suppression of the HIF-1α/PPAR-γ/PKM2 axis. Conclusions: Simvastatin can inhibit the HIF-1α/PPAR-γ/PKM2 axis, by suppressing PKM2-mediated glycolysis, resulting in decreased proliferation and increased apoptosis in HCC cells, and re-sensitizing HCC cells to Sora.

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“…These findings indicated that 15d-PGJ(2) inhibits neuronal autophagy after cerebral I/R injury to protect neurons. Isorhamnetin improves acute fulminant hepatitis induced by concanavalin A (ConA) via the P38/PPARα pathway, thus inhibiting the expression of proteins associated with apoptosis and autophagy (Lu et al 2018). However, the present findings of androgen-deprived PCa cells led to a contradictory conclusion.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-337-3p suppresses cell viability, apoptosis, and autophagy by modulating PPARγ expression in androgen-dependent human prostate cancer

Wang

Duan

et al. 2020

All Life

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2020) MicroRNA-337-3p suppresses cell viability, apoptosis, and autophagy by modulating PPARγ expression in androgendependent human prostate cancer, All Life, 13:1, 171-182, ABSTRACTWe proposed that autophagy activated through PPARγ in prostate cancer could protect cancer against androgen deprivation. Our MTT and western blotting assay results showed that mimics of miR-337-3p repressed autophagy flux under androgen deprivation, whereas inhibitors had the opposite effect. Neither mimics nor inhibitors influenced cell motility and invasion. miR-337-3p downregulated PPARγ expression in dual luciferase reporter assays and promoted AMPK phosphorylation. The overexpression of PPARγ or AMPK agonists partly diminished the adverse influence of mimics on proliferation and cell autophagy. In a mouse xenograft model, tumors transplanted with LNCap cells having a miR-337-3p deficiency had a significantly larger volume and lower rate of apoptosis than in controls after orchidectomy. Our findings showed that the negative effects of miR-337-3p on cell survival after androgen deprivation through PPARγ degeneration and modulated autophagy could serve as a novel therapeutic target for androgen-dependent prostate cancer and provide a strategy against resistance to anti-androgen therapy. ARTICLE HISTORY

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Isorhamnetin: A hepatoprotective flavonoid inhibits apoptosis and autophagy via P38/PPAR-α pathway in mice

Cited by 68 publications

References 42 publications

Therapeutic potential of PPARγ natural agonists in liver diseases

Therapeutic potential of PPARγ natural agonists in liver diseases

Simvastatin re-sensitizes hepatocellular carcinoma cells to sorafenib by inhibiting HIF-1α/PPAR-γ/PKM2-mediated glycolysis

MicroRNA-337-3p suppresses cell viability, apoptosis, and autophagy by modulating PPARγ expression in androgen-dependent human prostate cancer

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