scholarly journals Salvianolic Acid B Activates Chondrocytes Autophagy and Reduces Chondrocyte Apoptosis in Obese Mice via the KCNQ1OT1/Mir-128-3p/SIRT1 Signaling Pathways

2021 ◽  
Author(s):  
Tianwen Sun ◽  
Fei Wang ◽  
Gaojian Hu ◽  
Zhizhou Li
Keyword(s):  
Inflammatory Response ◽  
Cartilage Damage ◽  
Underlying Mechanism ◽  
Salvianolic Acid B ◽  
Sirtuin 1 ◽  
Chondrocyte Apoptosis ◽  
Standard Diet ◽  
Inflammatory Factor ◽  
Salvianolic Acid ◽  
Reduced Body

Abstract Purpose: Salvianolic acid B (Sal B) possesses strong anti-inflammatory and antioxidant activity. This study aims to explore the underlying mechanism of Sal B to improve the obesity-related osteoarthritis (OA). Methods: C57BL/6J male mice were fed with a standard diet, a high fat diet (HFD), or HFD with Sal B (25 mg/kg), and mouse body weights and osteoarticular inflammatory factor levels were examined. Mouse chondrogenic cell line ATDC5 were transfected with lncRNA KCNQ1 overlapping transcript 1 small hairpin RNA (KCNQ1OT1 shRNA), miR-128-3p mimic or Sirtuin-1 small interfering RNA (SIRT1 siRNA), then stimulated with Palmitic acid (PA) followed by the treatment of Sal B. Then, inflammatory response, apoptosis, and autophagy of ATDC5 cells in different groups were detected. Results: Sal B reduced body weight, decreased the levels of inflammatory markers, and improved cartilage damage in OA mice. KCNQ1OT1 was downregulated in OA mice and PA- stimulated ATDC5 cells. Sal B protected ATDC5 cells against PA-mediated inflammation, apoptosis, and the inhibition of autophagy, while knockdown of KCNQ1OT1 reversed these results. KCNQ1OT1 was found to be functioned as a ceRNA to bind and downregulate the expression of miR-128-3p that was upregulated in PA-induced cells. Furthermore, SIRT1 was verified as a target of miR-128-3p. MiR-128-3p overexpression reversed the effects of Sal B on inflammatory response, apoptosis, and autophagy in PA-stimulated cells, and knockdown of SIRT1 displayed similar results. Conclusion: Sal B exerted a chondroprotective effect by upregulating KCNQ1OT1, which indicates Sal B can used for a therapeutic agent in obesity-related OA.

scholarly journals Salvianolic Acid B Attenuates Apoptosis of HUVEC Cells Treated with High Glucose or High Fat via Sirt1 Activation

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jinghui Zhai ◽  
Lina Tao ◽  
Yueming Zhang ◽  
Huan Gao ◽  
Xiaoyu Qu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Umbilical Vein ◽  
Salvianolic Acid B ◽  
Sirtuin 1 ◽  
High Fat ◽  
Salvianolic Acid ◽  
Huvec Cells ◽  
Diabetic Cardiopathy

High glucose and high fat are important inducements for the development and progression of diabetic cardiopathy. Salvianolic acid B (SAB), which is the most abundant and bioactive compound in Danshen, attenuates oxidative stress-related disorders, such as cardiovascular diseases, cerebral ischemia, and diabetes. However, the effect of SAB on diabetic cardiopathy is not clear. The aim of study was to investigate the effect and the underlying molecular mechanisms of SAB on diabetic cardiopathy in vitro model. The human umbilical vein endothelial (HUVEC) cells were treated with high glucose (HG, 30 mM) or high fat (palmitic acid, PA, 0.75 mM) in the presence or absence of SAB (100, 200, and 400 mg/L) and incubated for 24 h. We found that HG or PA induced apoptosis of HUVEC cells, while treatment with SAB inhibited the apoptosis. We also found that SAB reversed HG- or PA-induced oxidative stress, apoptosis cell cytokines production, and expression of thioredoxin-interacting protein (TXNIP). Moreover, SAB increased HG- or PA-induced expression of Sirtuin 1 (Sirt1), a nicotinamide adenine dinucleotide- (NAD+-) dependent histone deacetylase. Exposure of HUVEC cells to Ex527 (Sirt1 inhibitor) suppressed the effect of SAB on acetyl-p53 and procaspase-3 expressions. In conclusion, the results suggested that SAB could attenuate HUVEC cells damage treated with HG or PA via Sirt1 and might be a potential therapy agent for the diabetic cardiopathy treatment.

scholarly journals Retraction: Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signaling pathway in IL-1β-induced osteoarthritis chondrocytes

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4441-4441
Author(s):  
Laura Fisher
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Akt Signaling ◽  
Salvianolic Acid B ◽  
Signalling Pathway ◽  
Akt Signaling Pathway ◽  
Salvianolic Acid ◽  
Osteoarthritis Chondrocytes

Retraction of ‘Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signalling pathway in IL-1β-induced osteoarthritis chondrocytes’ by Bin Zhu et al., RSC Adv., 2018, 8, 36422–36429, DOI: 10.1039/C8RA02418A.

Cardioprotection of salvianolic acid B and ginsenoside Rg1 combination on subacute myocardial infarction and the underlying mechanism

Phytomedicine ◽  
2019 ◽  
Vol 57 ◽  
pp. 255-261 ◽  
Author(s):  
Yuanmin Li ◽  
Linlin Wang ◽  
Zhihui Dong ◽  
Shiying Wang ◽  
Lili Qi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Underlying Mechanism ◽  
Salvianolic Acid B ◽  
Ginsenoside Rg1 ◽  
Salvianolic Acid

Salvianolic acid B exerts a protective effect in acute liver injury by regulating the Nrf2/HO-1 signaling pathway

2020 ◽  
Vol 98 (3) ◽  
pp. 162-168 ◽  
Author(s):  
Yong-mei Jin ◽  
Xiang-ming Tao ◽  
Yi-ning Shi ◽  
Youjin Lu ◽  
Jin-yu Mei
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Acute Liver Injury ◽  
Damage Model ◽  
Underlying Mechanism ◽  
Salvianolic Acid B ◽  
Salvianolic Acid ◽  
Injury Model

Salvianolic acid B (Sal B) exerts strong antioxidant activity and eliminates the free radical effect. However, how it affects the antioxidant pathway is not very clear. The objective of this study was to investigate the underlying mechanism of Sal B in CCl4-induced acute liver injury, especially its effect on the Nrf2/HO-1 signaling pathway. For the in vivo experiment, an acute liver injury model was induced using CCl4 and treated with Sal B. For the in vitro experiment, an oxidative damage model was established followed by Sal B treatment. Serum biochemical indicators and reactive oxygen species activity were detected using corresponding kits. Oxidant/antioxidant status was determined based on the levels of malondialdehyde, glutathione, and superoxide dismutase. Nrf2 and HO-1 levels were analyzed by Western blotting and immunohistochemical staining. Sal B treatment improved liver histology, decreased the aminotransferase levels, and attenuated oxidative stress in the acute liver injury model. Nrf2 and HO-1 levels were increased both in vivo and in vitro. Sal B suppresses acute liver injury and Nrf2/HO-1 signaling plays a key role in this process.

Salvianolic acid B prevents body weight gain and regulates gut microbiota and LPS/TLR4 signaling pathway in high-fat diet-induced obese mice

2020 ◽  
Vol 11 (10) ◽  
pp. 8743-8756
Author(s):  
Lin Li ◽  
Rui Li ◽  
Ruyuan Zhu ◽  
Beibei Chen ◽  
Yimiao Tian ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Body Weight Gain ◽  
Underlying Mechanism ◽  
Salvianolic Acid B ◽  
Obese Mice ◽  
Salvianolic Acid ◽  
Tlr4 Signaling Pathway ◽  
Metabolic Endotoxemia

Salvianolic acid B prevents body weight gain and improves insulin sensitivity in obese mice. The underlying mechanism behind these effects may be associated with the regulation of metabolic endotoxemia, gut microbiota homeostasis and LPS/TLR4 pathway.

scholarly journals Metformin Alleviates Steatohepatitis in Diet-Induced Obese Mice in a SIRT1-Dependent Way

2021 ◽  
Vol 12 ◽  
Author(s):  
Wan-rong Guo ◽  
Juan Liu ◽  
Li-dan Cheng ◽  
Zi-yu Liu ◽  
Xiao-bin Zheng ◽  
...  
Keyword(s):  
Body Weight ◽  
Hepatic Steatosis ◽  
Cholesterol Metabolism ◽  
Uncoupling Protein ◽  
Underlying Mechanism ◽  
Vital Role ◽  
Sirtuin 1 ◽  
Dependent Manner ◽  
Nonalcoholic Fatty Liver ◽  
Reduced Body

Metformin is the first-line anti-diabetic drug for type 2 diabetes. It has been found to significantly reduce liver aminotransferase in nonalcoholic fatty liver disease (NAFLD). However, whether metformin improves NAFLD progression remains controversial. Sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, plays a vital role in hepatic steatosis and inflammation. Here, we investigated the effect of metformin on steatohepatitis and the role of SIRT1 in diet-induced obese (DIO) mice. The results showed that metformin significantly reduced body weight and fat mass of DIO mice. In addition, metformin also alleviated adiposity and hepatic steatosis, and greatly upregulated uncoupling protein 1 (UCP1) expression in adipose tissues of DIO mice. Unexpectedly, the effects of metformin on reducing body weight and alleviating hepatic steatosis were not impaired in Sirt1 heterozygous knockout (Sirt1+/−) mice. However, SIRT1-deficiency remarkably impaired the effects of metformin on lowering serum transaminases levels, downregulating the mRNA expression of proinflammatory factors, and increasing the protein level of hepatic Cholesterol 25-Hydroxylase (CH25H), a cholesterol hydroxylase in cholesterol catabolism. In summary, we demonstrated that metformin alleviates steatohepatitis in a SIRT1-dependent manner, and modulation of M1 polarization and cholesterol metabolism may be the underlying mechanism.

Salvianolic acid B inhibits platelets-mediated inflammatory response in vascular endothelial cells

2015 ◽  
Vol 135 (1) ◽  
pp. 137-145 ◽  
Author(s):  
Shixin Xu ◽  
Aiqin Zhong ◽  
Xiaokun Bu ◽  
Huining Ma ◽  
Wei Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Response ◽  
Vascular Endothelial Cells ◽  
Salvianolic Acid B ◽  
Vascular Endothelial ◽  
Salvianolic Acid

scholarly journals Elevated expression of MMP8 and MMP9 contributes to diabetic osteoarthritis progression in a rat model

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Simin Luo ◽  
Wuji Li ◽  
Wenrui Wu ◽  
Qiping Shi
Keyword(s):  
High Fat Diet ◽  
Collagen Type ◽  
Morphological Changes ◽  
Cartilage Damage ◽  
Underlying Mechanism ◽  
Collagen Type I ◽  
Chondrocyte Apoptosis ◽  
Type I ◽  
High Fat ◽  
Differentiation Markers

Abstract Background Knowledge regarding the pathogenesis of osteoarthritis (OA) is very limited. Previous studies have shown that matrix metalloproteinase (MMP) 8 and MMP9 were upregulated in patients with diabetic OA. However, their regulatory functions and mechanisms in diabetic OA are not fully understood. Methods Diabetic OA rats were constructed using a high-fat diet combined with streptozotocin (STZ) induction. Safranin O-Fast green staining was used to detect the pathological changes in rat knee cartilage. MMP8 and MMP9 overexpression vectors or siRNAs were injected into diabetic OA rats to overexpress or knockdown the expression of MMP8 and MMP9, which was verified by real-time quantitative PCR (RT-qPCR). The expression of MMP8 and MMP9, chondrocyte differentiation markers collagen type II alpha 1 (COL2A1) and collagen type I alpha 1(COL1A1), and antiapoptotic protein BCL2 were detected using immunohistochemistry (IHC), and the number of apoptotic cells was detected by the transferase-mediated d-UTP nick-end-labeling (TUNEL) assay. Results High-fat diet combined with STZ-induced rats exhibited joint cartilage damage, morphological changes, and increased expression of MMP8 and MMP9. Overexpression of MMP8 and MMP9 in the joint cavity further aggravated the pathological morphological changes, decreased the expression of COL2A1 and COL1A1, increased the expression of BCL2, and promoted cell apoptosis in diabetic OA rats. The use of siRNA to inhibit MMP8 and MMP9 levels in the cartilage joints significantly reversed the decrease in COL2A1 and COL1A1 expression and partially reversed BCL2 expression and chondrocyte apoptosis. Conclusion MMP8 and MMP9 promoted rat diabetic OA model. The underlying mechanism may be related to inhibiting cartilage differentiation and promoting chondrocyte apoptosis.

scholarly journals Cardiovascular Effects of Salvianolic Acid B

2013 ◽  
Vol 2013 ◽  
pp. 1-16 ◽  
Author(s):  
Jie Wang ◽  
Xingjiang Xiong ◽  
Bo Feng
Keyword(s):  
Phenolic Acids ◽  
Salvia Miltiorrhiza ◽  
Cardiovascular Effects ◽  
Underlying Mechanism ◽  
Salvianolic Acid B ◽  
Asian Countries ◽  
Biological Mechanisms ◽  
Clinical Therapy ◽  
Salvianolic Acid ◽  
Cardioprotective Effects

Salvianolic acid B (SAB, Sal B) is the representative component of phenolic acids derived from the dried root and rhizome ofSalvia miltiorrhizaBge (Labiatae) which has been used widely and successfully in Asian countries for clinical therapy of various vascular disturbance-related diseases for hundreds of years. However, its exact cardioprotective components and the underlying mechanism for therapeutic basis are still poorly understood. This paper discussed and elucidated the underlying biological mechanisms and pharmacology of Sal B and their potential cardioprotective effects.

scholarly journals Salvianolic Acid B Protects Against Myocardial Ischemic Injury Through Inhibiting Apoptosis and Promoting Autophagy

2020 ◽  
Author(s):  
Chao Lin ◽  
Qi Chen ◽  
Linxiu Peng ◽  
Xiao Wu ◽  
Yongming Li ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Salvia Miltiorrhiza ◽  
Ischemic Injury ◽  
Underlying Mechanism ◽  
Salvianolic Acid B ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Related Factors ◽  
Salvianolic Acid ◽  
Myocardial Ischemic Injury

Abstract Aim of the study: Salvianolic acid B(Sal B) as a natural compound extracted from Salvia miltiorrhiza, has been extensively used to protect cardiomyocytes from myocardial ischemia. Although Sal B has shown evident effects on cardiovascular diseases, the detailed mechanism is still unclear as yet. Herein, we intended to explorethe protective effects of Sal B on myocardial ischemic injury and the underlying mechanism. Methods and Results: Western blotting, immunofluorescence assay, flow cytometry and lentiviral transfection were performed. The mice with myocardial ischemic injury were intravenously given 10 mg/kg Sal B once daily for seven days, and then H9c2 cells were treated with Sal B (20, 40, 80 μmol/L). Sal B treatment protected cardiomyocytes from myocardial ischemia through relieving apoptosis. Transmission electron microscopy and fluorescence microscopy exhibited that Sal B significantly increased autophagic lysosomes and vacuoles in H9c2 cells. Administration with Sal B significantly up-regulated the expressions of autophagy-related factors such as LC3, Atg5 and Beclin 1 in H9c2 cells and myocardial tissues. The beneficial autophagic changes induced by Sal B were abrogated through pharmacological inhibition. Conclusions: This study provides a molecular mechanism by which Sal B potently inhibits apoptosis and oxidative stress upon myocardial ischemia by activating the AMPK-autophagy pathway. Sal B is a potential agent for treating myocardial ischemia.

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