&lt;p&gt;Salidroside-Mitigated Inflammatory Injury of Hepatocytes with Non-Alcoholic Fatty Liver Disease via Inhibition TRPM2 Ion Channel Activation&lt;/p&gt;

Qi, Feng; Liu, Chen; Gao, Wei; Geng, Xiaoling; Dai, Ning

doi:10.2147/dmso.s210764

Cited by 21 publications

(26 citation statements)

References 44 publications

(47 reference statements)

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“…The pharmacological effects of salidroside include, but not limited to, anti-cancer (Rong et al, 2020), anti-inflammatory (Pu et al, 2020), anti-hypoxia (Chen, Kou, Lu, & Pu, 2020), and anti-oxidative properties (Liu et al, 2020). Recent pieces of evidence demonstrated that salidroside has also been considered as a potential therapeutic drug for diabetes because of its beneficial action in diabetic rodent models (Feng, Liu, Gao, Geng, & Dai, 2019). However, the specific molecular mechanism is remaining unclear.…”

Section: Introductionmentioning

confidence: 99%

Retracted : Salidroside from Rhodiola wallichiana var. cholaensis reverses insulin resistance and stimulates the GLP‐1 secretion by alleviating ROS‐mediated activation of MAPKs signaling pathway and mitigating apoptosis

Yan

Nian

et al. 2020

J. Food Biochem.

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The present study was aimed to investigate the mechanisms of salidroside (SAL) from Rhodiola wallichiana var. cholaensis on hypoglycemic and oxidative stress responses. The palmitate (PA)-induced GLUTag cells model and the glucosamine-induced insulin resistance model in HepG2 cells were built. SAL led to the up-regulation of the serum glucagon-like peptide 1 (GLP-1) level by facilitating the SCFAs production, the promotion of GLP-1 synthesis by improving p38 MAPK phosphorylation and regulating insulin resistance. Moreover, the production of reactive oxygen species (ROS) and the expression of MAPKs were down-regulated. Furthermore, SAL was found to be able to inhibit PA-induced apoptosis that down-regulates cleaved caspase-3 and Bax expressions, while up-regulating Bcl-2 expression and up-regulates the Bcl-2/ Bax ratio in glucosamine induced insulin resistance model. Besides, SAL can also upregulate the mTOR/p70S6k signaling pathway in the PA-induced GLUTag cells model. Our data demonstrated that SAL could reverse insulin resistance and stimulates the GLP-1 secretion by alleviating ROS-mediated activation of MAPKs signaling pathway and mitigating apoptosis. Practical applications Our data showed that SAL could increase the GLP-1 level by stimulating the SCFAs production and p38 phosphorylation and facilitate the IR and GLP-1 synthesis by alleviating ROS-mediated activation of MAPKs signaling pathway and mitigating apoptosis. Furthermore, the SAL has also stimulated the mTOR/p70S6k signaling pathway in PA-induced GLUTag cells model. The results provided a possibility to employ SAL for diabetes treatment.

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Section: Introductionmentioning

confidence: 99%

Retracted : Salidroside from Rhodiola wallichiana var. cholaensis reverses insulin resistance and stimulates the GLP‐1 secretion by alleviating ROS‐mediated activation of MAPKs signaling pathway and mitigating apoptosis

Yan

Nian

et al. 2020

J. Food Biochem.

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“…An in vitro study revealed that Heshouwu ( Fallopia multiflora ) could alleviate NAFLD by promoting mitochondrial β oxidation and attenuating lipid accumulation in L02 human liver cells [ 136 ]. Moreover, salidroside, a phenylpropanoid glycoside compound from Hongjingtian ( Rhodiola rosea ), could ameliorate NAFLD in L02 cells through alleviating steatosis and inflammation, as well as activating autophagy by downregulating the transient receptor potential melastatin2-Ca 2+ -calmodulin-stimulated protein kinase II (TRPM2-Ca 2+ -CaMKII) signaling pathway [ 137 ]. Furthermore, the treatment of silybin could alleviate NAFLD in FaO liver cells by increasing the expression of PPAR- α / δ and decreasing the expression of PPAR- γ [ 138 ].…”

Section: Mechanisms Of Plant-based Foods and Their Bioactive Compomentioning

confidence: 99%

Plant-Based Foods and Their Bioactive Compounds on Fatty Liver Disease: Effects, Mechanisms, and Clinical Application

Gan

Shang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Fatty liver disease (FLD), including nonalcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (AFLD), is a serious chronic metabolic disease that affects a wide range of people. Lipid accumulation accompanied by oxidative stress and inflammation in the liver is the most important pathogenesis of FLD. The plant-based, high-fiber, and low-fat diet has been recommended to manage FLD for a long time. This review discusses the current state of the art into the effects, mechanisms, and clinical application of plant-based foods in NAFLD and AFLD, with highlighting related molecular mechanisms. Epidemiological evidence revealed that the consumption of several plant-based foods was beneficial to alleviating FLD. Further experimental studies found out that fruits, spices, teas, coffee, and other plants, as well as their bioactive compounds, such as resveratrol, anthocyanin, curcumin, and tea polyphenols, could alleviate FLD by ameliorating hepatic steatosis, oxidative stress, inflammation, gut dysbiosis, and apoptosis, as well as regulating autophagy and ethanol metabolism. More importantly, clinical trials confirmed the beneficial effects of plant-based foods on patients with fatty liver. However, several issues need to be further studied especially the safety and effective doses of plant-based foods and their bioactive compounds. Overall, certain plant-based foods are promising natural sources of bioactive compounds to prevent and alleviate fatty liver disease.

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“…There is suggestive evidence that TRPM2 channel activity may be altered in steatotic hepatocytes and hence may contribute to the progression of non-alcoholic fatty liver disease to cirrhosis and hepatocellular carcinoma [ 93 ]. Feng and colleagues employed an “in vitro model of non-alcoholic fatty liver disease” comprised of immortalised LO2 liver cells in culture loaded with lipids by incubation with palmitate.…”

Section: Trpm2 Channels In Liver Cells May Be Involved In Non-alcoholic Fatty Liver Disease and Its Progression To Cirrhosis And Hepatocementioning

confidence: 99%

“…These palmitate-induced changes were all reduced by saliroside. The authors concluded that the observed actions of saliroside are due to inhibition of expression of TRPM2 and subsequent reduction in [Ca 2+ ] cyt , leading to decreased activation of Ca 2+ /calmodulin-dependent protein kinase II, increased autophagy, and decreased inflammation [ 93 ].…”

Section: Trpm2 Channels In Liver Cells May Be Involved In Non-alcoholic Fatty Liver Disease and Its Progression To Cirrhosis And Hepatocementioning

confidence: 99%

TRPM2 Non-Selective Cation Channels in Liver Injury Mediated by Reactive Oxygen Species

2021

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TRPM2 channels admit Ca2+ and Na+ across the plasma membrane and release Ca2+ and Zn2+ from lysosomes. Channel activation is initiated by reactive oxygen species (ROS), leading to a subsequent increase in ADP-ribose and the binding of ADP-ribose to an allosteric site in the cytosolic NUDT9 homology domain. In many animal cell types, Ca2+ entry via TRPM2 channels mediates ROS-initiated cell injury and death. The aim of this review is to summarise the current knowledge of the roles of TRPM2 and Ca2+ in the initiation and progression of chronic liver diseases and acute liver injury. Studies to date provide evidence that TRPM2-mediated Ca2+ entry contributes to drug-induced liver toxicity, ischemia–reperfusion injury, and the progression of non-alcoholic fatty liver disease to cirrhosis, fibrosis, and hepatocellular carcinoma. Of particular current interest are the steps involved in the activation of TRPM2 in hepatocytes following an increase in ROS, the downstream pathways activated by the resultant increase in intracellular Ca2+, and the chronology of these events. An apparent contradiction exists between these roles of TRPM2 and the role identified for ROS-activated TRPM2 in heart muscle and in some other cell types in promoting Ca2+-activated mitochondrial ATP synthesis and cell survival. Inhibition of TRPM2 by curcumin and other “natural” compounds offers an attractive strategy for inhibiting ROS-induced liver cell injury. In conclusion, while it has been established that ROS-initiated activation of TRPM2 contributes to both acute and chronic liver injury, considerable further research is needed to elucidate the mechanisms involved, and the conditions under which pharmacological inhibition of TRPM2 can be an effective clinical strategy to reduce ROS-initiated liver injury.

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<p>Salidroside-Mitigated Inflammatory Injury of Hepatocytes with Non-Alcoholic Fatty Liver Disease via Inhibition TRPM2 Ion Channel Activation</p>

Cited by 21 publications

References 44 publications

Retracted : Salidroside from Rhodiola wallichiana var. cholaensis reverses insulin resistance and stimulates the GLP‐1 secretion by alleviating ROS‐mediated activation of MAPKs signaling pathway and mitigating apoptosis

Retracted : Salidroside from Rhodiola wallichiana var. cholaensis reverses insulin resistance and stimulates the GLP‐1 secretion by alleviating ROS‐mediated activation of MAPKs signaling pathway and mitigating apoptosis

Plant-Based Foods and Their Bioactive Compounds on Fatty Liver Disease: Effects, Mechanisms, and Clinical Application

TRPM2 Non-Selective Cation Channels in Liver Injury Mediated by Reactive Oxygen Species

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