scholarly journals Salvianolic Acid B Improves Chronic Mild Stress-Induced Depressive Behaviors in Rats: Involvement of AMPK/SIRT1 Signaling Pathway

2020 ◽  
Vol Volume 13 ◽  
pp. 195-206 ◽  
Author(s):  
Dehua Liao ◽  
Yun Chen ◽  
Yujin Guo ◽  
Changshui Wang ◽  
Ni Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Chronic Mild Stress ◽  
Salvianolic Acid B ◽  
Mild Stress ◽  
Salvianolic Acid

scholarly journals Salvianolic acid B ameliorates depressive-like behaviors in chronic mild stress-treated mice: involvement of the neuroinflammatory pathway

2016 ◽  
Vol 37 (9) ◽  
pp. 1141-1153 ◽  
Author(s):  
Jin-qiang Zhang ◽  
Xiao-hui Wu ◽  
Yi Feng ◽  
Xiao-fang Xie ◽  
Yong-hua Fan ◽  
...  
Keyword(s):  
Chronic Mild Stress ◽  
Salvianolic Acid B ◽  
Mild Stress ◽  
Salvianolic Acid

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.

scholarly journals Salvianolic Acid B Improves Postresuscitation Myocardial and Cerebral Outcomes in a Murine Model of Cardiac Arrest: Involvement of Nrf2 Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Qing-Qi Ji ◽  
Yan-Jie Li ◽  
Ying-Hua Wang ◽  
Zi Wang ◽  
Liang Fang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Signaling Pathway ◽  
Murine Model ◽  
Nuclear Translocation ◽  
Salvia Miltiorrhiza ◽  
Left Ventricular ◽  
Salvianolic Acid B ◽  
Mitochondrial Morphology ◽  
Salvianolic Acid ◽  
Nrf2 Signaling Pathway

Survival and outcome of cardiac arrest (CA) are dismal despite improvements in cardiopulmonary resuscitation (CPR). Salvianolic acid B (Sal B), extracted from Salvia miltiorrhiza, has been investigated for its cardioprotective properties in cardiac remodeling and ischemic heart disease, but less is known about its role in CA. The aim of this study was to learn whether Sal B improves cardiac and neurologic outcomes after CA/CPR in mice. Female C57BL/6 mice were subjected to eight minutes of CA induced by an intravenous injection of potassium chloride (KCl), followed by CPR. After 30 seconds of CPR, mice were blindly randomized to receive either Sal B (20 mg/kg) or vehicle (normal saline) intravenously. Hemodynamic variables and indices of left ventricular function were determined before CA and within three hours after CPR, the early postresuscitation period. Sal B administration resulted in a remarkable decrease in the time required for the return of spontaneous circulation (ROSC) in animals that successfully resuscitated compared to the vehicle-treated mice. Myocardial performance, including cardiac output and left ventricular systolic (dp/dtmax) and diastolic (dp/dtmin) function, was clearly ameliorated within three hours of ROSC in the Sal B-treated mice. Moreover, Sal B inhibited CA/CPR-induced cardiomyocyte apoptosis and preserved mitochondrial morphology and function. Mechanistically, Sal B dramatically promoted Nrf2 nuclear translocation through the downregulation of Keap1, which resulted in the expression of antioxidant enzymes, including HO-1 and NQO1, thereby counteracted the oxidative damage in response to CA/CPR. The aforementioned antiapoptotic and antioxidant effects of Sal B were impaired in the setting of gene silencing of Nrf2 with siRNA in vitro model. These improvements were associated with better neurological function and increased survival rate (75% vs. 40%, p<0.05) up to 72 hours postresuscitation. Our findings suggest that the administration of Sal B improved cardiac function and neurological outcomes in a murine model of CA via activating the Nrf2 antioxidant signaling pathway, which may represent a novel therapeutic strategy for the treatment of CA.

Regulation of SIRT3/FOXO1 Signaling Pathway in Rats with Non-alcoholic Steatohepatitis by Salvianolic Acid B

2017 ◽  
Vol 48 (6) ◽  
pp. 506-512 ◽  
Author(s):  
Yingchun Wang ◽  
Juan Chen ◽  
Weizong Kong ◽  
Ruiping Zhu ◽  
Kai Liang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Salvianolic Acid B ◽  
Salvianolic Acid ◽  
Alcoholic Steatohepatitis

scholarly journals Intervention Effect of Compatibility of Salvianolic Acid A & B on PDGF-C/PDGFR-α Signaling Pathway in Renal Fibrosis

2015 ◽  
Vol 4 (2) ◽  
pp. 13
Author(s):  
Bin Yu
Keyword(s):  
Signaling Pathway ◽  
Renal Fibrosis ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Salvianolic Acid B ◽  
Control Group ◽  
Salvianolic Acid ◽  
Salvianolic Acid A ◽  
Drug Compatibility ◽  
Renal Tubular

<strong>Objective</strong>: To explore the effect of salvianolic acid A &amp; B component molecules of drug compatibility on PDGF-c/PDGFR-α signaling pathway in renal fibrosis of rats. <strong>Methods</strong>: 40 male SPF SD rats were randomly divided into four groups: control group, salvianolic acid A group, salvianolic acid B group and salvianolic acid A + B group, with 10 rats in each group. Each group was treated for two weeks. After the intervention, samples were collected. And scores of HE and Masson was compared. The expression of PDGF-c/PDGFR-α in rental tissue in them was also tested and compared.<strong> Results</strong>: Compared with the control group, the score of HE and Masson in intervention groups was markedly decreased, and scores in salvianolic acid B group and salvianolic acid A + B group were reduced significantly (<em>p </em>&lt; 0.05); Compared with the control group, the expression of PDGF-c/PDGFR-α in rental tissue in intervention groups was lower(<em>p </em>&lt; 0.05), especially in salvianolic acid B group and salvianolic acid A + B group (<em>p </em>&lt; 0.05).<strong>Conclusion</strong>: salvianolic acid A &amp; B component molecules of drug compatibility could significantly improve the pathological changes in the kidney tissue of rats, suppress the expression of PDGF-c/PDGFR-α in renal tissue, and improve the renal function, renal tubular function and renal pathology.

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.

scholarly journals Effects of Chronic Mild Stress on the Development of Atherosclerosis and Expression of Toll-Like Receptor 4 Signaling Pathway in Adolescent Apolipoprotein E Knockout Mice

2009 ◽  
Vol 2009 ◽  
pp. 1-13 ◽  
Author(s):  
Hongfeng Gu ◽  
Chaoke Tang ◽  
Kuang Peng ◽  
Hui Sun ◽  
Yongzong Yang
Keyword(s):  
Apolipoprotein E ◽  
Signaling Pathway ◽  
Knockout Mice ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Apolipoprotein E Knockout Mice ◽  
Tlr4 Signaling Pathway ◽  
Myeloid Differentiation Factor

Here, we investigated the effect of chronic mild stress (CMS) on the development of atherosclerosis as well as the expression of Toll-like receptors (TLRs) signaling pathway in adolescent apolipoprotein E knockout (apoE-/-) mice. Mice were subjected to daily CMS for 0, 4, and 12 weeks, respectively. To identify the expression of Toll-like receptor 4 signaling pathway in adolescent apolipoprotein E knockout mice subjected to CMS, we compared gene expression in aortas of stressed and unstressed mice using TLRs signaling pathway real-time PCR microarrays consisting of 87 genes. We found that atherosclerosis lesions both in aortic tress and sinuses of CMS mice were significantly increased linearly in response to duration of CMS exposure. Among 87 genes analyzed, 15 genes were upregulated in stressed mice, especially TLR4, myeloid differentiation factor 88 (MyD88), and IL-1β, and 28 genes were downregulated compared with nonstressed mice. CMS mice demonstrated markedly increased aortic atherosclerosis that were associated with significant increases in levels of expression of TLR4, MyD88, nuclear factorκB (NF-κB), MCP-1, IL-1β, TNF-α, and sICAM-1. Taken together, our results suggest an important role for TLR4 signaling pathway in atherosclerosis in a CMS mouse model.

Sign in / Sign up

Export Citation Format

Share Document