Salidroside alleviates high glucose-induced oxidative stress and extracellular matrix accumulation in rat glomerular mesangial cells by the TXNIP-NLRP3 inflammasome pathway

Wang, Shiying; Zhao, Xinxin; Yang, Suxia; Chen, Baoping; Shi, Jun

doi:10.1016/j.cbi.2017.10.012

Cited by 80 publications

(39 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The induction was inhibited by astilbin ( Figures 1C,D ). Based on these results and a previous study (Wang et al, 2017), 24 h was selected as treatment time in the following experiments.…”

Section: Resultsmentioning

confidence: 99%

Astilbin Inhibits High Glucose-Induced Inflammation and Extracellular Matrix Accumulation by Suppressing the TLR4/MyD88/NF-κB Pathway in Rat Glomerular Mesangial Cells

et al. 2018

View full text Add to dashboard Cite

Diabetic nephropathy (DN) is characterized by inflammatory responses and extracellular matrix (ECM) accumulation. Astilbin is an active natural compound and possesses anti-inflammatory activity. The aim of this study was to evaluate the anti-inflammatory effect of astilbin on high glucose (HG)-induced glomerular mesangial cells and the potential mechanisms. The results showed that HG induced cell proliferation of HBZY-1 cells in a time-dependent manner, and astilbin inhibited HG-induced cell proliferation. The expression and secretion of inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), and ECM components, including collagen IV (Col IV) and fibronectin (FN), were induced by HG. Moreover, TGF-β1 and CTGF were also induced by HG. The induction by HG on inflammatory response and ECM accumulation was inhibited after astilbin treatment. Astilbin treatment also attenuated HG-induced decrease in expression of matrix metalloproteinase (MMP)-2 and MMP-9. The TLR4/MyD88/NF-κB pathway was activated by HG, and the inhibitor of TLR4 exhibited the same effect to astilbin on reversing the induction of HG. TLR4 overexpression attenuated the effect of astilbin on HG-induced inflammatory cytokine production and ECM accumulation. The results suggested that astilbin attenuated inflammation and ECM accumulation in HG-induced rat glomerular mesangial cells via inhibiting the TLR4/MyD88/NF-κB pathway. This work provided evidence that astilbin can be considered as a potential candidate for DN therapy.

show abstract

“…The induction was inhibited by astilbin ( Figures 1C,D ). Based on these results and a previous study (Wang et al, 2017), 24 h was selected as treatment time in the following experiments.…”

Section: Resultsmentioning

confidence: 99%

Astilbin Inhibits High Glucose-Induced Inflammation and Extracellular Matrix Accumulation by Suppressing the TLR4/MyD88/NF-κB Pathway in Rat Glomerular Mesangial Cells

et al. 2018

View full text Add to dashboard Cite

show abstract

“…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, ). Using other animal models and isolated renal cells, authors have attributed that the anti‐oxidant and anti‐apoptotic effect of Salidroside could be secondary to the hypoglycemic effect or due to other direct effects such as inhibition of inflammation and activation of anti‐oxidant and anti‐apoptotic pathways such as SIRT1 (Li et al, ; Lu et al, ; Wang et al, ; Xue et al, ; Yin et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…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, ). Using other animal models and isolated renal cells, authors have attributed that the anti‐oxidant and anti‐apoptotic effect of Salidroside could be secondary to the hypoglycemic effect or due to other direct effects such as inhibition of inflammation and activation of anti‐oxidant and anti‐apoptotic pathways such as SIRT1 (Li et al, ; Lu et al, ; Wang et al, ; Xue et al, ; Yin et al, ). Most recently, Salidroside protected pancreatic β‐cells from diabetes‐associated oxidative stress via activating the AMPK pathway (Ju et al, ).…”

Section: Discussionmentioning

confidence: 99%

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

Shati

2020

J Food Biochem

View full text Add to dashboard Cite

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.

show abstract

“…It has also previously been suggested that AQP5 may affect cell proliferation and migration during tumor development. For example, downregulating AQP5 expression inhibited the proliferation and migration of human gastric carcinoma cells (22), human glioma cells (23) and prostate cancer cells (24). Downregulating AQP5 in Ishikawa cells has also been shown to reduce cell migration (25).…”

Section: Discussionmentioning

confidence: 99%

Differential expression and inhibitory effects of aquaporins on the development of adenomyosis

et al. 2020

View full text Add to dashboard Cite

aquaporin 2 (aQP2), aQP5 and aQP8 participate in adenomyosis (AM). Ηowever, the roles of these three molecules in AM have not been fully elucidated. In the present study, Institute of Cancer Research female mice were used to establish a model of AM. Subsequently, the endometrial tissues of the mice were observed by hematoxylin-eosin staining, and AM severity, uterus diameter, uterus index, ovary index and numbers of nodules on the uterine surface were evaluated and counted. In addition, eutopic and ectopic endometrial stromal cells (ESCs) were isolated from eutopic and ectopic endometrial samples derived from patients with AM and were then identified by immunofluorescence. The viability, and migratory and invasive ability of ESCs transfected with small interfering RNA targeting AQP5 (siAQP5) were determined by Cell Counting Κit-8, scratch wound-healing and Transwell assays, respectively. Reverse transcription-quantitative polymerase chain reaction was performed to determine the mRNA expression levels of AQP5, epithelial-mesenchymal transition (EMT)-related genes (E-and N-cadherin), matrix metalloproteinase (MMP)-2 and-9. Protein expression levels of AQP2, AQP5, AQP8, E-, N-cadherin, MMP-2 and-9 were detected by western blotting. AM severity and uterus index were higher, and there were a greater number of nodules on the uterine surface in the AM group compared with the sham group. AQP2, AQP5 and AQP8 proteins were highly expressed in eutopic and ectopic endometrium of the AM group, and AQP5 was more highly expressed than AQP2 or AQP8. In addition, the data showed that Vimentin was positively expressed in ESCs, and that siAQP5 suppressed the mRNA expression levels of AQP5, cell viability, migration, invasion, EMT and MMP-2 and-9 expression in ESCs. In conclusion, AQP2, AQP5 and AQP8 were highly expressed in eutopic and ectopic endometrium. Notably, AQP5 silencing may suppress AM by inhibiting viability, migration, invasion, EMT, and MMP-2 and-9 expression in ESCs.

show abstract

Salidroside alleviates high glucose-induced oxidative stress and extracellular matrix accumulation in rat glomerular mesangial cells by the TXNIP-NLRP3 inflammasome pathway

Cited by 80 publications

References 25 publications

Astilbin Inhibits High Glucose-Induced Inflammation and Extracellular Matrix Accumulation by Suppressing the TLR4/MyD88/NF-κB Pathway in Rat Glomerular Mesangial Cells

Astilbin Inhibits High Glucose-Induced Inflammation and Extracellular Matrix Accumulation by Suppressing the TLR4/MyD88/NF-κB Pathway in Rat Glomerular Mesangial Cells

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

Differential expression and inhibitory effects of aquaporins on the development of adenomyosis

Contact Info

Product

Resources

About