Acute kidney injury

AMP-activated protein kinase regulates autophagic protection against cisplatin-induced tissue injury in the kidney

L. Wei, Chen, W., Zou, Y., Huang, H., Pan, B., Jin, S., Huang, R., Nie, S., and Kong, G., AMP-activated protein kinase regulates autophagic protection against cisplatin-induced tissue injury in the kidney, vol. 14, pp. 12006-12015, 2015.

Although the nephrotoxicity of cisplatin has been well documented as a major side effect of chemotherapy, the exact mechanism by which prosurvival and apoptotic pathways interplay to determine renal pathology remains elusive. Recent studies suggested that autophagy might serve as an adaptive mechanism to promote cell survival during acute kidney injury (AKI). We have used AKI as a disease model to investigate the mechanism regulating the cytoprotective role of autophagy in cisplatin-induced tissue damage.

Protective effect of penehyclidine hydrochloride on lipopolysaccharide-induced acute kidney injury in rat

H. J. Cao, Yu, D. M., Zhang, T. Z., Zhou, J., Chen, K. Y., Ge, J., and Pei, L., Protective effect of penehyclidine hydrochloride on lipopolysaccharide-induced acute kidney injury in rat, vol. 14, pp. 9334-9342, 2015.

We aimed to observe the effect of penehyclidine hydrochloride (PHC) on lipopolysaccharide (LPS)-induced acute kidney injury in rats and expression of tight junction proteins ZO-1 and occludin. Adult male Sprague-Dawley (SD) rats were divided randomly (N = 10) into control group (C), LPS group (LPS), low-dose PHC group (L-PHC), and high-dose PHC group (H-PHC). All rats, except C group, received a vena caudalis injection of 5.0 mg/kg LPS; after 30 min, rats in L-PHC and H-PHC groups received a vena caudalis injection of 0.3 and 0.9 mg/kg PHC.

Subscribe to Acute kidney injury