AI Article Synopsis
- - The study examines how the stress protein heme oxygenase-1 (HO-1) impacts endoplasmic reticulum stress (ERS) in rat liver cells (hepatocytes) when exposed to lipopolysaccharide (LPS).
- - Researchers treated cultured rat hepatocyte cells with various combinations of LPS and HO-1 interference methods, measuring cell health and expression of specific stress-related proteins.
- - Findings indicated that LPS increased HO-1 levels and worsened cell injury and apoptosis; however, blocking HO-1 with siRNA led to even more severe ERS and cell damage, suggesting that HO-1 plays a protective role against LPS-induced injury.
Article Abstract
Objective: To investigate effects of antioxidant stress protein heme oxygenase-1 (HO-1) on lipopolysaccharide (LPS)-induced endoplasmic reticulum stress (ERS) of rat hepatocytes.
Methods: The BRL cells (rat hepatocyte cell line) were cultured. The hepatocytes were treated with LPS, LPS+HO-1 siRNA, HO-1 siRNA and PBS solution, respectively. The cell viability was measured by trypan blue exclusion test. The apoptosis cells were detected by the fluorescent dye Hoechst 33258. Expressions of GRP78, CHOP, caspase-12 and HO-1 were detected by Western blotting.
Results: LPS caused an increase of HO-1 protein expression of rat hepatocytes in a dose-dependent and time-dependent manner, a up-regulation of GRP78, CHOP and caspase-12, a decrease in cell viability, and an increase in apoptosis rate of hepatocytes. Pretreatment of HO-1 siRNA inhibited the up-regulation of LPS-induced HO-1, however, aggravated ERS and cellular injury.
Conclusion: HO-1 inhibites ERS-mediated cellular injury of rat hepatocytes induced by LPS.
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