Anti-insulin resistance effects of salidroside through mitochondrial quality control

You, Baiyang; Dun, Yaoshan; Zhang, Wenliang; Jiang, Ling; Li, Hui; Xie, Murong; Liu, Yuan; Liu, Suixin

doi:10.1530/joe-19-0393

Cited by 16 publications

(12 citation statements)

References 47 publications

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“…10 The autophagy process is dependent on a multitude of signaling pathways. Adenosine monophosphate activated protein kinase (AMPK) functions as a regulator of cell energy metabolism, [12][13][14] and phosphorylated AMPK (pAMPK) plays a key role in autophagy. 15 Mammalian target of rapamycin (mTOR), as one of the main autophagy inhibitory pathways, also plays an important role in the occurrence of autophagy.…”

Section: Introductionmentioning

confidence: 99%

<p>Galangin Improved Non-Alcoholic Fatty Liver Disease in Mice by Promoting Autophagy</p>

Zhang¹,

Deng²,

Xiang³

et al. 2020

DDDT

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Background: Previous studies have shown that curcumin derivatives can improve the fatty degeneration of liver tissue that occurs in nonalcoholic fatty liver disease (NAFLD). However, the specific mechanism for that improvement remains unclear. We examined whether the curcumin derivative galangin could reduce the fatty degeneration of liver tissue in mice with NAFLD by inducing autophagy, from the perspective of both prevention and treatment. Methods: C57BL/6J mice were randomly assigned to a prevention group (given galangin and a HFD simultaneously) or a treatment group (given galangin after being fed an HFD). The prevention group was treated with galangin (100 mg/kg/d) or an equal volume of normal saline (NS) while being fed an HFD. Some mice were treated with an autophagy inhibitor (3-methyladenine, 3-MA; 30 mg/kg/biwk, i.p.) while being fed an HFD and galangin. HepG2 cells were cultured in DMEM medium containing both free fatty acids and galangin. Results: Galangin was found to reduce the fatty degeneration of liver tissue induced by eating an HFD at both the prevention and treatment levels, and that effect might be related to an enhancement of hepatocyte autophagy. Inhibition of autophagy by 3-MA blocked the protective effect of galangin on hepatic steatosis. At the cellular level, galangin reduced lipid accumulation and enhanced the level of hepatocyte autophagy. Conclusion: In vitro and in vivo studies showed that galangin cannot only improve preexisting hepatic steatosis but also prevent the development of stenosis by promoting hepatocyte autophagy.

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Section: Introductionmentioning

confidence: 99%

<p>Galangin Improved Non-Alcoholic Fatty Liver Disease in Mice by Promoting Autophagy</p>

Zhang¹,

Deng²,

Xiang³

et al. 2020

DDDT

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“…It ameliorates muscle atrophy in cachexia or denervation via activating mTOR signaling pathway or reducing expression of atrogenes, such as MuRF1 and Atrogin-1 (Chen et al, 2016;Wu et al, 2019). Our previous study also indicated that salidroside resists metabolic disorders in skeletal muscle via upregulating SIRT1-mediated mitochondrial quality control in mice (You et al, 2020). Our present study further showed that in skeletal muscle cells, salidroside abated palmitate-induced SIRT1 inhibition, atrogenes activation, and myotubes atrophy and these therapeutic effects were significantly attenuated by additional EX-527 pre-treatment.…”

Section: Discussionmentioning

confidence: 92%

The Treatment of Rhodiola Mimics Exercise to Resist High-Fat Diet-Induced Muscle Dysfunction via Sirtuin1-Dependent Mechanisms

You

Dun

et al. 2021

Front. Pharmacol.

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Muscle dysfunction is a complication of high-fat diet (HFD)-induced obesity that could be prevented by exercise, but patients did not get enough therapeutic efficacy from exercise due to multiple reasons. To explore alternative or supplementary approaches to prevent or treat muscle dysfunction in individuals with obesity, we investigated the effects of Rhodiola on muscle dysfunction as exercise pills. SIRT1 might suppress atrogenes expression and improve mitochondrial quality control, which could be a therapeutic target stimulated by exercise and Rhodiola, but further mechanisms remain unclear. We verified the lipid metabolism disorders and skeletal muscle dysfunction in HFD feeding mice. Moreover, exercise and Rhodiola were used to intervene mice with a HFD. Our results showed that exercise and Rhodiola prevented muscle atrophy and dysfunction in obese mice and activating the SIRT1 pathway, while atrogenes were suppressed and mitochondrial quality control was improved. EX-527, SIRT1 inhibitor, was used to validate the essential role of SIRT1 in salidroside benefit. Results of cell culture experiment showed that salidroside alleviated high palmitate-induced atrophy and mitochondrial quality control impairments, but these improvements of salidroside were inhibited by EX-527 in C2C12 myotubes. Overall, Rhodiola mimics exercise that activates SIRT1 signaling leading to improvement of HFD-induced muscle dysfunction.

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“…reported that SAL alleviated glucosamine‐induced insulin resistance in HepG2 cells in a dose‐dependent manner [39] . In addition, SAL was found to reduce insulin resistance and regulate mitochondrial quality control and ROS production by activating AMPK/silent information regulator 1 (SIRT1) signaling pathway [40] …”

Section: Pharmacological Activity and Mechanism Of Sal Against Metabolic Diseasesmentioning

confidence: 99%

“…[39] In addition, SAL was found to reduce insulin resistance and regulate mitochondrial quality control and ROS production by activating AMPK/silent information regulator 1 (SIRT1) signaling pathway. [40]…”

Section: Effect Of Sal On Insulin Resistancementioning

confidence: 99%

The Therapeutic Effects and Mechanisms of Salidroside on Cardiovascular and Metabolic Diseases: An Updated Review

Zhao

Huan

et al. 2021

Chemistry & Biodiversity

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The increasing incidence of metabolic and cardiovascular diseases has severely affected global human health and life safety. In recent years, some effective drugs with remarkable curative effects and few side effects found in natural compounds have attracted attention. Salidroside (SAL), a phenylpropane glycoside, is the main active ingredient of the plateau plant Rhodiola. So far, many animal experiments proved that SAL has good biological activity against some metabolic and cardiovascular diseases. However, most of these reports are scattered. This review systematically summarizes the pharmacological progress of SAL in the treatment of several metabolic (e. g., diabetes and non-alcoholic fatty liver disease) and cardiovascular (e. g., atherosclerosis) diseases in a timely manner to promote the clinical application and basic research of SAL. Accumulating evidence proves that SAL has beneficial effects on these diseases. It can improve glucose tolerance, insulin sensitivity, and β-cell and liver functions, and inhibit adipogenesis, inflammation and oxidative stress. Overall, SAL may be a valuable and potential drug candidate for the treatment of metabolic and cardiovascular diseases. However, more studies especially clinical trials are needed to further confirm its therapeutic effects and molecular mechanisms.

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Anti-insulin resistance effects of salidroside through mitochondrial quality control

Cited by 16 publications

References 47 publications

<p>Galangin Improved Non-Alcoholic Fatty Liver Disease in Mice by Promoting Autophagy</p>

<p>Galangin Improved Non-Alcoholic Fatty Liver Disease in Mice by Promoting Autophagy</p>

The Treatment of Rhodiola Mimics Exercise to Resist High-Fat Diet-Induced Muscle Dysfunction via Sirtuin1-Dependent Mechanisms

The Therapeutic Effects and Mechanisms of Salidroside on Cardiovascular and Metabolic Diseases: An Updated Review

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