Cerebral Protection of Salvianolic Acid A by the Inhibition of Granulocyte Adherence

2011 ◽  
Vol 39 (01) ◽  
pp. 111-120 ◽  
Author(s):  
Min Jiang ◽  
Xiao-Ying Wang ◽  
Wang-Yi Zhou ◽  
Jing Li ◽  
Jie Wang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Vascular Endothelial Cells ◽  
Leukocyte Adhesion ◽  
Ischemia Reperfusion ◽  
Experimental Studies ◽  
Cerebral Protection ◽  
Active Components ◽  
Salvianolic Acid ◽  
Salvianolic Acid A ◽  
Adhesion Rate

Ischemic stroke is one of the most common causes of death and disability that is induced by ischemia reperfusion (IR). Granulocyte adherence has been proven to be a principal cause of IR. Salvianolic acid A (Sal A) is one of the major active components of Danshen, a Chinese herbal medicine used for the treatment of cardiovascular and cerebrovascular diseases, such as ischemic stroke. Some experimental studies have shown the strong cerebral protection effect of Sal A. However, little information is available about the effect of Sal A on granulocyte adherence to brain micro-vascular endothelial cells (BMEC). Therefore, the aim of the present study was to investigate the effect of Sal A on the leukocyte adhesion rate and the intercellular cell adhesion molecule-1 (ICAM-1) expression in BMEC injured by hypoxia/reoxygenation (H/R), using a rheometer, qRT-PCR, and flow cytometry (FCM). The results of the adhesion rate gathered by the rheometer showed that Sal A could remarkably inhibit the adherence of granulocytes on BMEC in the case of H/R injury. Moreover, PCR and FCM results showed that Sal A could decrease the expression of ICAM-1 on BMEC on the gene and protein levels. In conclusion, the study demonstrated that the inhibition of granulocyte adherence is one of the targets of Sal A in the treatment of ischemic stroke. Meanwhile, Sal A inhibits of granulocyte adherence by decreasing the expression of ICAM-1 in BMEC.

scholarly journals Salvianolic Acid A Protects Against Oxidative Stress and Apoptosis Induced by Intestinal Ischemia-Reperfusion Injury Through Activation of Nrf2/HO-1 Pathways

2018 ◽  
Vol 49 (6) ◽  
pp. 2320-2332 ◽  
Author(s):  
Guo Zu ◽  
Tingting Zhou ◽  
Ningwei Che ◽  
Xiangwen Zhang
Keyword(s):  
Reactive Oxygen Species ◽  
Glutathione Peroxidase ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Salvianolic Acid ◽  
Salvianolic Acid A ◽  
Tnf Α

Background/Aims: Ischemia-reperfusion (I/R) adversely affects the intestinal mucosa. The major mechanisms of I/R are the generation of reactive oxygen species (ROS) and apoptosis. Salvianolic acid A (SalA) is suggested to be an effective antioxidative and antiapoptotic agent in numerous pathological injuries. The present study investigated the protective role of SalA in I/R of the intestine. Methods: Adult male Sprague-Dawley rats were subjected to intestinal I/R injury in vivo. In vitro experiments were performed in IEC-6 cells subjected to hypoxia/ reoxygenation (H/R) stimulation to simulate intestinal I/R. TNF-α, IL-1β, and IL-6 levels were measured using enzyme-linked immunosorbent assay. Malondialdehyde and myeloperoxidase and glutathione peroxidase levels were measured using biochemical analysis. Apoptosis was measured by terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling staining or flow cytometry in vivo and in vitro. The level of reactive oxygen species (ROS) was measured by dichlorodihydrofluorescin diacetate (DCFH-DA) staining. Western blotting was performed to determine the expression of heme oxygenase-1 (HO-1), Nrf2 and proteins associated with apoptosis. The mRNA expressions of Nrf2 and HO-1 were detected by quantitative real-time polymerase chain reaction in vivo and in vitro. Results: Malondialdehyde level and myeloperoxidase and glutathione peroxidase, TNF-α, IL-1β, and IL-6 levels group in intestinal tissue decreased significantly in the SalA pretreatment groups compared to the I/R group. SalA markedly abolished intestinal injury compared to the I/R group. SalA significantly attenuated apoptosis and increased Nrf2/HO-1 expression in vivo and in vitro. However, Nrf2 siRNA treatment partially abrogated the above mentioned effects of SalA in H/R-induced ROS and apoptosis in IEC-6 cells. Conclusion: The present study demonstrated that SalA ameliorated oxidation, inhibited the release of pro-inflammatory cytokines and alleviated apoptosis in I/R-induced injury and that these protective effects may partially occur via regulation of the Nrf2/ HO-1 pathways.

Salvianolic acid a attenuates limb ischemia/reperfusion injury in skeletal muscle of rats

2018 ◽  
Vol 97 ◽  
pp. 551-556 ◽  
Author(s):  
Yijia Xiang ◽  
Shiyong Ye ◽  
Changhong Cai ◽  
Junchong Chen ◽  
Xuyong Zhao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Salvianolic Acid ◽  
Salvianolic Acid A

scholarly journals Cardioprotective Effects of Salvianolic Acid A on Myocardial Ischemia-Reperfusion InjuryIn VivoandIn Vitro

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Huaying Fan ◽  
Liu Yang ◽  
Fenghua Fu ◽  
Hui Xu ◽  
Qinggang Meng ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Salvianolic Acid ◽  
Salvianolic Acid A ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Salvianolic acid A (SAA), one of the major active components of Danshen that is a traditional Chinese medicine, has been reported to possess protective effect in cardiac diseases and antioxidative activity. This study aims to investigate the cardioprotection of SAAin vivoandin vitrousing the model of myocardial ischemia-reperfusion in rat and hydrogen peroxide (H2O2)-induced H9c2 rat cardiomyoblasts apoptosis. It was found that SAA significantly limited infarct size of ischemic myocardium when given immediately prior to reperfusion. SAA also significantly suppressed cellular injury and apoptotic cell death. Additionally, the results of western blot and phospho-specific antibody microarray analysis showed that SAA could up-regulate Bcl-2 expression and increase the phosphorylation of proteins such as Akt, p42/p44 extracellular signal-related kinases (Erk1/2), and their related effectors. The phosphorylation of those points was related to suppress apoptosis. In summary, SAA possesses marked protective effect on myocardial ischemia-reperfusion injury, which is related to its ability to reduce myocardial cell apoptosis and damage induced by oxidative stress. The protection is achieved via up-regulation of Bcl-2 expression and affecting protein phosphorylation. These findings indicate that SAA may be of value in cardioprotection during myocardial ischemia-reperfusion injury, which provide pharmacological evidence for clinical application.

scholarly journals Pharmacokinetic and metabolomic analyses of the neuroprotective effects of salvianolic acid A in a rat ischemic stroke model

2017 ◽  
Vol 38 (11) ◽  
pp. 1435-1444 ◽  
Author(s):  
Si-qi Feng ◽  
Nan Aa ◽  
Jian-liang Geng ◽  
Jing-qiu Huang ◽  
Run-bin Sun ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Stroke Model ◽  
Neuroprotective Effects ◽  
Salvianolic Acid ◽  
Salvianolic Acid A

scholarly journals Salvianolic acid A ameliorates renal ischemia/reperfusion injury by activating Akt/mTOR/4EBP1 signaling pathway

2018 ◽  
Vol 315 (2) ◽  
pp. F254-F262 ◽  
Author(s):  
Ying Song ◽  
Weihai Liu ◽  
Yi Ding ◽  
Yanyan Jia ◽  
Jinyi Zhao ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Initiation Factor ◽  
Salvianolic Acid ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Salvianolic Acid A

Salvianolic acid A (Sal A) has been shown to prevent and treat ischemic cardiovascular, as well as cerebral vascular diseases. However, little is known about Sal A in renal ischemia/reperfusion (I/R) injury. In this study, a renal I/R injury model in rats and a hypoxia/reoxygenation (H/R) model to damage proximal renal tubular cells (HK-2) were used to assess whether Sal A halts the development and progression of renal I/R injury. As compared with vehicle treatment, Sal A significantly attenuated kidney injury after renal I/R injury, accompanied by decreases in plasma creatinine, blood urea nitrogen levels, the number of apoptosis-positive tubular cells, and kidney oxidative stress. Sal A also activated phosphorylated protein kinase B (p-Akt) and phosphorylated-mammalian target of rapamycin (p-mTOR) compared with vehicle-treated I/R injury rats. In H/R-injured HK-2 cells, Sal A can reduce the levels of reactive oxygen species in a dose-related manner. Similar to the results from in vivo experiments, in vitro Sal A also increased the protein expression of phosphorylated-eukaryotic initiation factor 4E binding protein 1 (p-4EBP1) compared with vehicle. Furthermore, the cytoprotective activity of Sal A was inhibited by LY294002 and rapamycin. These findings indicate that Sal A can ameliorate renal I/R injury and promote tubular cell survival partly via the Akt/mTOR/4EBP1pathway. Sal A could be a candidate compound to prevent ischemic tissue damage.

Sign in / Sign up

Export Citation Format

Share Document