Tetrahydroxystilbene glucoside alleviates Ang Ⅱ-induced senescence of HUVECs via SIRT1

Tetrahydroxystilbene glucoside (TSG), an active ingredient of <i>Polygonum multiflorum</i>, has been known for certain anti-aging effects. In this study, the possible protective mechanism of TSG on human umbilical vein endothelial cells (HUVECs) senescence induced by angiotensin Ⅱ (Ang Ⅱ) was investigated. The results revealed that TSG pretreatment could reduce the percentage of senescence-associated-β-galactosidase (SA-β-gal) positive cells, and decrease the expression levels of the cellular senescence biomarkers, p53 and PAI-1 proteins. At the same time, the expression of SIRT1 in senescent cell showed an upward trend due to TSG treatment. When inhibiting the expression of SIRT1 by EX527, our results showed that TSG reversed the effect of EX527, by promoting the expression level of SIRT1, reducing the expression of SA-β-gal positive cell and the expression level of p53 and PAI-1 proteins. The present study demonstrated that TSG could protect against HUVECs senescence induced by Ang Ⅱ, potentially through modulation of SIRT1 activity.

Tetrahydroxystilbene Glucoside Suppresses NAPDH Oxidative Stress to Mitigate Apoptosis and Autophagy Induced by Cerebral Ischemia/Reperfusion Injury in Mice

Tetrahydroxystilbene glucoside (TSG) is the active ingredient extracted from the traditional Chinese medicine Fallopia multiflora, which has extensive pharmacological activities. The current study aimed to observe the neuroprotective mechanism of TSG in the ischemia/reperfusion (I/R) brain injury-induced apoptosis and autophagy from the point of view of oxidative stress (OS). The middle cerebral artery occlusion (MCAO) model was prepared through the suture-occluded method, and TSG was administered through tail vein injection at the time of reperfusion at the doses of 3.0, 6.0, and 12.0 mg/kg. Compared with sham group, the neurological score in I/R mice was increased (P<0.05), along with remarkably elevated cerebral infarct volume (P<0.05); while TSG administration could reduce the neurological score and cerebral infarct volume (P<0.05) and improve the neuronal damage in ischemic cortex and hippocampus (P<0.05). The expression of NOX4, activated caspase-3(9), and Beclin 1 (P<0.05), as well as the LC3BII/I ratio, had been markedly elevated (P<0.05), while TSG administration could effectively suppress the expression of the above-mentioned proteins (P<0.05). In conclusion, TSG shows obvious protection against brain injury in I/R mice, and its mechanism may be related to suppressing the NADPH-induced OS and reducing neuronal apoptosis as well as autophagy.