Protective Effects of Salidroside against Carbon Tetrachloride (CCl4)-Induced Liver Injury by Initiating Mitochondria to Resist Oxidative Stress in Mice

Lin, Shiyu; Xu, Danning; Du, Xiaxia; Ran, Chonglin; Lu, Xu; Ren, Shao-Jun; Tang, Zongxi; Yin, Lizi; He, Chao; Yuan, Zhixiang; Fu, Hualin; Zhao, Xiaoling; Shu, Gang

doi:10.3390/ijms20133187

Cited by 47 publications

(33 citation statements)

References 51 publications

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“…Herein, Salidroside nephroprotective effect was also associated with antioxidant and an anti-apoptotic mechanisms as evident by the significantly reduction in the levels ROS, lipid peroxidation (MDA), In the same line to our findings, Salidroside also increased the activity of SOD, GPx and CAT activities in the livers and kidneys of alloxan-induced diabetic mice (Li et al, 2008). Also, the antioxidant and anti-apoptotic effects of Salidroside were shown to be the major mechanism protecting the liver, heart, lung, and kidney from oxidative stress-induced damage in other animal models (Chen et al, 2019;Guo et al, 2018;Lai et al, 2014;Lin et al, 2019). LG-treated cells (Lane I).…”

Section: F I G U R Esupporting

confidence: 88%

“…In the same line to our findings, Salidroside also increased the activity of SOD, GPx and CAT activities in the livers and kidneys of alloxan‐induced diabetic mice (Li et al, ). Also, the antioxidant and anti‐apoptotic effects of Salidroside were shown to be the major mechanism protecting the liver, heart, lung, and kidney from oxidative stress‐induced damage in other animal models (Chen et al, ; Guo et al, ; Lai et al, ; Lin et al, ). In addition, Salidroside inhibited HG‐induced induced mesangial cell and podocytes apoptosis via inhibition of oxidative stress (Lu et al, ; Wang, Zhao, Yang, Chen, & Shi, ; Yin et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…On the contrary, the medical therapeutic potential of Salidroside [(4‐hydroxy‐phenethyl)‐β‐D‐glucopyranoside, a glycosides of Rhodiola rosea (R. rosea L) is well reported in various organs of different animal model with many thanks to antioxidant, anti‐inflammatory, and anti‐apoptotic effects (Chen, Lin, Qi, He, & Zheng, ; Lai et al, ; Lin et al, ; Yin, Yao, Chen, Hu, & Gao, ). Of note, Salidroside attenuated hyperlipidemia, insulin resistance (IR), and renal damage in mice model of T2DM and db/db diabetic mice (Wang et al, ; Wu et al, ; Xue et al, ; Zheng et al, ) and improved kidney function and reduced renal cell apoptosis in streptozotocin (STZ) plus uninephrectomy induced diabetic rats (Guo et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Salidroside ameliorates diabetic nephropathy in rats by activating renal AMPK/SIRT1 signaling pathway

Shati

2020

J Food Biochem

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This study investigated if the nephroprotective effect of Salidroside T1DM rats involves activation of AMPK/SIRT1. Rats were divided into control or T1DM and treated with vehicle or Salidroside (100 mg/kg) for 56 days. Mesangial cells were cultured in LG or HG media with or without Salidroside (100 µM/L) for 24 hr. Also, HG + Salidroside‐treated cells were pre‐incubated with EX‐527 or compound C (CC) for 1 hr. With reducing glucose levels, Salidroside improved kidney structure/function in the T1DM rat. It also increased GSH and Bcl‐2 levels in control and T1DM rats and inhibited ROS, increased activation of AMPK and nuclear SIRT1, and lowered acetylation of P53 and FOXO‐1 in control and T1DM rats and in LG and HG‐treated cells. These effects were abolished by EX‐527 and CC. Also, CC decreased the nuclear levels of SIRT1. In conclusion, Salidroside attenuates DN in T1DM rats by activation of AMPK and subsequently, SIRT1. Practical applications This animal and pre‐clinical study shows that Salidroside is able to ameliorate DN in T1DM‐induced rats and showed that it mainly acts by a hypoglycemic effect and activation of renal AMPK/SIRT1 axis. Given the wide tissue stimulatory effect of AMPK on peripheral glucose utilization, lipogenesis, and other cell signaling pathways, these data are encouraging to investigate the anti‐diabetic effect of glycoside in more clinical trials.

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Section: F I G U R Esupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Salidroside ameliorates diabetic nephropathy in rats by activating renal AMPK/SIRT1 signaling pathway

Shati

2020

J Food Biochem

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“…14 Multiple lines of evidence suggested that Sal could effectively improve liver diseases induced by some chemical toxins. [15][16][17][18] Studies also show that Sal markedly protected against inflammatory injury of hepatocytes with NAFLD through scavenging ROS production. 19…”

Section: Introductionmentioning

confidence: 96%

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

Qi¹,

Liu²,

Gao³

et al. 2019

DMSO

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Purpose: Oxidative stress plays an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). TRPM2 ion channel functions as a molecular sensor for oxidative stress. The aim of this study was to examine the protective effects of Salidroside, a powerful antioxidative plant, on TRPM2 in an established in vitro model of NAFLD. Methods: NAFLD model was established by palmitic acid (PA) in hepatic L02 cell lines and was added to the media at a final concentration of 400 μM. Cells were used as normal group, PA group and PA receiving varied concentrations of Salidroside (75μg/mL, 150μg/ mL, 300μg/mL). After treating 24 hrs, MTT assay was used to detect cell viability, and ALT level was measured using an appropriate kit assay. Intracellular lipid accumulation was observed by Oil red O staining. Cytosolic Ca 2+ concentrations were evaluated by flow cytometer with Fluo-3/AM. Quantitative RT-PCR was used to measure the mRNA expression of TRPM2, IL-1β and IL-6, and the protein expressions of TRPM2, p-CaMKII and autophagy (LC3B, p62) were determined using Western blot. Results: Treatment with Salidroside effectively restored liver injury and alleviated lipid droplet deposition in a dose-dependent manner, which was associated with inhibition of TRPM2/Ca 2+ /CaMKII pathway. Additionally, autophagic clearance was enhanced by intervention with Salidroside in a dose-dependent manner. Further investigation indicated that Salidroside down-regulated the mRNA expression of IL-1β and IL-6-pro-inflammatory cytokines. Conclusion: These results suggest that Salidroside could alleviate inflammatory injury and steatosis via autophagy activation mediated by downregulation of the TRPM2/Ca 2+ /CaMKII pathway. Targeting the TRPM2 ion channel is a novel treatment strategy for oxidative stressinduced liver in NAFLD.

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“…The mechanism of liver tissue injury is complex. It has been reported that free radicals or reactive oxygen species are the main factors responsible for liver injury (Lin, Dan, et al, 2019;Lu, Wang, Zhang, Liu, & Xu, 2017). Through lipid peroxidation of biological membranes, they cause damage to liver cell membranes, mitochondrial membranes and other biological membranes, resulting in degeneration and necrosis of liver cells, and an increase of lipid peroxides in the body (Kakuni et al, 2012;Rofiee et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Analysis of Streptococcus agalactiae ‐induced liver injury in tilapia ( Oreochromis niloticus )

Cao

Jia

et al. 2020

Aquac Res

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Streptococcosis, a bacterial disease for multiple fish species, especially tilapia, caused more disruption to the fish culture industry. However, the underlying mechanisms for the occurrence of streptococcosis remain unclear. The aim of this study was to study the effects of streptococcus on the liver of tilapia. In this study, tilapia were injected streptococcal solution (0.05 ml/10 g body weight) and collected blood and liver at 4, 8, 24, 48, 72, 96, 120 and 144 hr after injection. The results showed that the activities of glutamate oxalate transaminase (GOT), glutamate pyruvate transaminase (GPT), alkaline phosphatase (AKP) and superoxide dismutase (SOD) in the serum of tilapia exhibited irregular changes: increase at first, then decrease and increase again. The levels of total antioxidant capacity (T‐AOC), glutathione (GSH) and malondialdehyde (MDA) showed a decreasing tendency in serum after injection, except GSH at 4 hr. The activity of catalase (CAT) decreased in serum at 4, 24, 120 and 144 hr after injection of streptococcal solution, while the content TP enhanced in serum at 48, 72 and 120 hr after injection. Observations of pathological sections showed obvious damage to the liver tissue structure in response to streptococcal infection. Western blotting revealed an increase in ikkbeta (Ikkβ) protein with prolonged infection time and a decrease in NF‐kappa‐B inhibitor alpha (IkB‐α) and ikappab kinase alpha (Ikkα) proteins. The gene expression of cytochrome P4501A (CYP1A) was downregulated in liver at 24 and 48 after injection, while the mRNA levels of heat stress protein 70 (HSP70) and tumour necrosis factor alpha (TNF‐α) increased at 48 and/or 72 hr. Taken together, our findings confirmed that streptococcus can cause serious damage to the liver of tilapia.

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Protective Effects of Salidroside against Carbon Tetrachloride (CCl4)-Induced Liver Injury by Initiating Mitochondria to Resist Oxidative Stress in Mice

Cited by 47 publications

References 51 publications

Salidroside ameliorates diabetic nephropathy in rats by activating renal AMPK/SIRT1 signaling pathway

Salidroside ameliorates diabetic nephropathy in rats by activating renal AMPK/SIRT1 signaling pathway

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

Analysis of Streptococcus agalactiae ‐induced liver injury in tilapia ( Oreochromis niloticus )

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