Protective effects of salvianolic acid B against hydrogen peroxide‑induced apoptosis of human umbilical vein endothelial cells and underlying mechanisms

Abstract

Salvianolic acid B (Sal B) is a water-soluble active component of Danshen and has anti-atherosclerotic effects. The present study aimed to evaluate the cytoprotective effects of Sal B against hydrogen peroxide (H 2 O 2 )-induced oxidative stress damage in human umbilical vein endothelial cells (HUVECs) and investigate the underlying mechanisms. It was revealed that Sal B protected the cells from H 2 O 2 -induced damage, as indicated by MTT results showing enhanced cell viability and by flow cytometric analysis showing reduced apoptosis of cells challenged with H 2 O 2 . Furthermore, as an underlying mechanism, the enhancement of autophagy was indicated to be accountable for the decrease in apoptosis, as Sal B caused the upregulation of light chain 3-II and Beclin-1, and downregulation of p62 under H 2 O 2 -induced oxidative stress. Finally, Sal B increased the phosphorylation of AMP kinase (AMPK) and decreased the phosphorylation of mammalian target of rapamycin (mTOR), but had no effect on the phosphorylation of AKT. In conclusion, the present study revealed that Sal B protects HUVECs from oxidative stress, at least partially by promoting autophagy via activation of the AMPK pathway and downregulation of the mTOR pathway.

Pharmacokinetics of Active Ingredients of Salvia miltiorrhiza and Carthamus tinctorius in Compatibility in Normal and Cerebral Ischemia Rats: A Comparative Study

“…It is often used for the treatment of cardio-cerebral-vascular disease caused by blood stasis [30,44,45]. Existing studies have shown that DSS, SAA, SAB, and HSYA have the ability to scavenge free oxygen radicals, inhibit apoptosis, and prevent inflammation [5][6][7][8][9][10][11][12][13][14][15][16][17][18][25][26][27][28], thereby protecting against cerebral ischemic injury. Over the past few years, the Dan-Hong injection and its ingredients have been widely studied in clinical and basic research [30,[46][47][48].…”

“…SAA can scavenge free oxygen radicals [5,6] and has a protective effect on cell damage caused by oxidative stress [7,8]. SAB not only has strong antioxidant effects [9][10][11][12][13], but it can also inhibit apoptosis [14][15][16][17][18]. DSS is an important water-soluble ingredient, which has been pharmacologically shown to improve blood circulation [19] and eliminate blood stasis [20,21], and can also protect against cerebral ischemia reperfusion injury [22].…”

Silicon Oxynitrophosphide Nanoscale Coating Enhances Antioxidant Marker‐Induced Angiogenesis During in vivo Cranial Bone‐Defect Healing

“…The H2O2 has been used previously for in vitro studies (29)(30) (31) as a major product of oxidative stress, mainly produced by swift conversion from superoxide (32)(33) (34) . Based on previous publications, this specific H2O2 concentration has been demonstrated to be deleterious to live tissue (19) (20) .…”

Plant-Derived Molecules α-Boswellic Acid Acetate, Praeruptorin-A, and Salvianolic Acid-B Have Age-Related Differential Effects in Young and Senescent Human Fibroblasts In Vitro

“…In contrast, a decrease of LC3BII levels was observed in ABC-, PTA-, and SAB-treated cells at early passage ( Figure 6A). SAB has been already established as an inducer of autophagy in different biological settings [34][35][36][37][38]. SAB-induced autophagy plays a pro-death role and contributed to the cell death of colorectal cancer cell lines through the suppression of AKT/mTOR pathway [35].…”

“…SAB also promotes cardioprotective effects in rat acute myocardial infarction model by the induction of expression of antioxidant enzyme SOD1, anti-apoptotic protein Bcl-2, and autophagy proteins, namely LC3-II and Beclin 1 [34]. SAB also protects human umbilical vein endothelial cells (HUVEC) against hydrogen peroxide-induced oxidative stress by promoting autophagy via the activation of AMPK pathway and the downregulation of mTOR pathway [37,38]. SAB also limits alpha-synuclein aggregation and induces chaperone-mediated autophagy in cellular models of alpha-synuclein aggregation [38].…”