2,3,5,4′‐Tetrahydroxystilbene‐2‐O‐β‐d‐glucoside eliminates ischemia/reperfusion injury–induced H9c2 cardiomyocytes apoptosis involving in Bcl‐2, Bax, caspase‐3, and Akt activation

Abstract

Objective: This study was designed to explore the protective effect of 2,3,5, 4′-tetrahydroxystilbene-2-O-β-D-glucoside (TSG) against ischemia/reperfusion (I/R) injury-induced cardiomyocytes apoptosis. Methods: The H9c2 cell I/R injury model was induced by simultaneous shortage of nutrients and oxygen. TSG administration (0.10, 0.25, and 0.50 mM) was performed before and during I/R stimulation. Cell apoptosis was evaluated using terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Expression of cell-related proteins was detected to assess the effect of TSG on cell apoptosis. Results: I/R injury induced significant cell apoptosis. Significantly decreased Bcl-2 and increased Bax, caspase-3, and p-Akt expression (P < 0.01) was detected in the cell model of I/R injury. In contrast, TSG administration eliminated all the changes induced by I/R injury in a dose-dependent manner. Compared with the H9c2 cell model of I/R injury, the H9c2 cells treated with 0.50 mM TSG showed the lowest cell apoptosis percentage, the highest expression of Bcl-2, and the lowest expression of Bax, caspase-3, and p-Akt (P < 0.01). Conclusion: We confirmed that the protective effect of TSG against I/R injuryinduced cell apoptosis in H9c2 in vitro was associated with the Bcl-2/Bax ratio, caspase-3, and Akt activation. K E Y W O R D S 2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-glucoside, apoptosis, H9c2, ischemia/reperfusion

Qiliqiangxin reduced cardiomyocytes apotosis and improved heart function in infarcted heart through Pink1/Parkin -mediated mitochondrial autophagy

“…The results showed that QLQX could significantly reduce the infarct area, improve the heart function and survival rate of mice at 28 days after surgery. Bcl-2-related protein family is the main regulator of cell apoptosis signal transduction pathway, and the ratio of anti-apoptosis protein Bcl-2 to pro-apoptosis protein Bax determines whether cells undergo apoptosis when stimulated by apoptosis signal [28,30]. Our study found that after ligation of left coronary artery, the expression of Bax increased significantly while the expression of Bcl-2 decreased significantly in MI + saline group compare to sham group.…”

“…Basic research shows that QLQX could restrain hypoxia-induced injury in primary rat cardiac microvascular endothelial cells via promoting glycolysis in a HIF-1a-dependent manner [27]. During hypoxia, cardiac microvascular endothelial cells (CMVECs) promote the expression of vascular endothelial growth factor (VEGF) and QLQX could attenuate this injury via facilitating hypoxia inducible factor-1α(HIF-1α)dependent glycolysis [28]. However, the mechanism of QLQX on apoptosis still remains unknown.…”

Simultaneous Determination of 13 Constituents of Radix Polygoni Multiflori in Rat Plasma and Its Application in a Pharmacokinetic Study

“…Stilbenes, mainly 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), possessed antioxidative, antitumor, anti-inflammatory, endothelial protective, neuroprotective, and liver-protective activities, etc. [10][11][12][13][14][15][16][17][18][19][20][21]. Anthraquinones were reported to possess many biological activities, including immunomodulating, anticancer, antimutation, antibacterial, anticancer, antioxidant, etc.…”

Couplet medicines of leech and centipede granules improve erectile dysfunction via inactivation of the CaSR/PLC/PKC signaling in streptozotocin-induced diabetic rats

“…Bcl-2 is a famous representative suppressor of apoptosis, while Bax can combine with Bcl-2 to form a heterodimer for antagonize the inhibitory effect of Bcl-2 on apoptosis and promote apoptosis [41]. On the other hand, Bax also activates caspase-3 with promoting the Ca 2+ release and then causes cell apoptosis [42]. Caspase-3 is as a representative executor plays a pivotal role in cell apoptosis.…”