Inhibition of HtrA2 alleviates inflammatory response and cell apoptosis in lipopolysaccharide ‑induced acute pneumonia in rats.

Inhibition of HtrA2 alleviates inflammatory response and cell apoptosis in lipopolysaccharide‑induced acute pneumonia in rats. Mol Med Rep. 2020 Aug 04;: Authors: Wang X Abstract Pneumonia is one of the commonest causes of death worldwide. High‑temperature requirement A2 (HtrA2) is a proapoptotic mitochondrial serine protease involved in caspase‑dependent or caspase‑independent cell apoptosis. UCF‑101 (5‑[5‑(2‑nitrophenyl) furfuryl iodine]‑1,3‑diphenyl‑2‑thiobarbituric acid), an inhibitor of HtrA2, has a protective effect on organs in various diseases by inhibiting cell apoptosis. The aim of the present study was to explore whether UCF‑101 has a protective effect on lungs in pneumonia. A lipopolysaccharide (LPS)‑induced pneumonia model was established in rats. UCF‑101 (2 µmol/kg) was used for treatment. Lung injury was detected by hematoxylin and eosin staining. Pro‑inflammatory cytokines and oxidative stress‑related factors were detected using corresponding test kits. TUNEL staining was used to measure the amount of cell apoptosis. Apoptosis‑associated proteins were detected by western blot assay. The present study indicated pulmonary injury induced by LPS. Treatment with UCF‑101 clearly alleviated this pulmonary damage and restored the levels of pro‑inflammatory cytokines and oxidative stress‑related factors. In addition, UCF‑101 significantly reduced LPS‑induced cell apoptosis, the ...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research