Salvianolic acid B protects hepatocytes from H2O2 injury by stabilizing the lysosomal membrane

• Published in: World journal of gastroenterology : WJG Vol. 23; no. 29; pp. 5333 - 5344
• Main Authors: Yan, Xiao-Feng, Zhao, Pei, Ma, Dong-Yan, Jiang, Yi-Lu, Luo, Jiao-Jiao, Liu, Liu, Wang, Xiao-Ling
• Format: Journal Article
• Language: English
• Published: Baishideng Publishing Group Inc 07.08.2017
• Subjects: Basic Study
• ISSN: 1007-9327; 2219-2840
• DOI: 10.3748/wjg.v23.i29.5333

AIM To investigate the capability of salvianolic acid B（Sal B） to protect hepatocytes from hydrogen peroxide（H2O2）/carbon tetrachloride（CCl4）-induced lysosomal membrane permeabilization. METHODS Cell Counting Kit-8 assay was used to measure cell viability. Apoptosis and death were assayed through flow cytometry. Brd U incorporation was used to detect cell proliferation. Serum alanine aminotransferase activity and liver malondialdehyde（MDA） content were measured. Liver histopathological changes were evaluated using hematoxylin-eosin staining. Lysosomal membrane permeability was detected with Lyso Tracker Green-labeled probes and acridine orange staining. The levels of protein carbonyl content（PCC）, cathepsins（Cat）B/D, and lysosome-associated membrane protein 1（LAMP1） were evaluated through western blotting. Cytosol Cat B activity analysis was performed with chemiluminescence detection. The m RNA level ofLAMP1 was evaluated through quantitative real-time polymerase chain reaction. RESULTS Results indicated that H2O2 induced cell injury/death. Sal B attenuated H2O2-induced cell apoptosis and death, restored the inhibition of proliferation, decreased the amount of PCC, and stabilized the lysosome membrane by increasing the LAMP1 protein level and antagonizing Cat B/D leakage into the cytosol. CCl4 also triggered hepatocyte death. Furthermore, Sal B effectively rescued hepatocytes by increasing LAMP1 expression and by reducing lysosomal enzyme translocation to the cytosol.CONCLUSION Sal B protected mouse embryonic hepatocytes from H2O2/CCl4-induced injury/death by stabilizing the lysosomal membrane.