Aconitine promotes ROS-activated P38/MAPK/Nrf2 pathway to inhibit autophagy and promote myocardial injury.

Background: Aconitine has cardiotoxicity, but the mechanism of cardiotoxicity induced by aconitine is limited. The aim of this study was to investigate the mechanism of myocardial injury induced by aconitine.

Methods: Using aconitine, ROS inhibitor N-acetylcysteine(NAC), the autophagy activitor Rapamycin (Rap) or the P38/MAPK pathway activitor Dehydrocorydaline treats H9C2 cells.

Aconitine Induces TRPV2-Mediated Ca Influx through the p38 MAPK Signal and Promotes Cardiomyocyte Apoptosis.

Aconitine is the main effective component of traditional Chinese medicine , which has been proved to have severe cardiovascular toxicity. The toxic effect of aconitine on cardiomyocytes is related to intracellular calcium overload, but the mechanism remains unclear. The aim of this study was to explore the mechanism of aconitine inducing intracellular Ca overload and promoting H9c2 cardiomyocyte apoptosis through transient receptor potential cation channel subfamily V member 2 (TRPV2).

Renal Tissue Damage Induced by Acute Kidney Injury in Sepsis Rat Model Is Inhibited by Cynaropicrin via IL-1β and TNF-α Down-Regulation.

Acute kidney injury (AKI), one of the frequently diagnosed and serious sepsis induced complication has high morbidity and mortality. The present study investigated the effect of cynaropicrin on AKI induced pathological damage in rat model in vivo. Treatment with cynaropicrin suppressed AKI induced urea nitrogen and creatinine in the rat serum in dose-dependent manner.

Thal protects against paraquat-induced lung injury through a microRNA-141/HDAC6/IκBα-NF-κB axis in rat and cell models.

The protective functions of thalidomide in paraquat (PQ)-induced injury have been reported. But the mechanisms remain largely unknown. In this research, a PQ-treated rat model was established and further treated with thalidomide.