Published online Aug 7, 2017. doi: 10.3748/wjg.v23.i29.5333
Peer-review started: January 19, 2017
First decision: February 23, 2017
Revised: March 27, 2017
Accepted: May 9, 2017
Article in press: May 9, 2017
Published online: August 7, 2017
Processing time: 201 Days and 11.9 Hours
To investigate the capability of salvianolic acid B (Sal B) to protect hepatocytes from hydrogen peroxide (H2O2)/carbon tetrachloride (CCl4)-induced lysosomal membrane permeabilization.
Cell Counting Kit-8 assay was used to measure cell viability. Apoptosis and death were assayed through flow cytometry. BrdU 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 LysoTracker 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 CatB activity analysis was performed with chemiluminescence detection. The mRNA level of LAMP1 was evaluated through quantitative real-time polymerase chain reaction.
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 CatB/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.
Sal B protected mouse embryonic hepatocytes from H2O2/CCl4-induced injury/death by stabilizing the lysosomal membrane.
Core tip: Lysosomal membrane permeabilization leads to the release of luminal contents, such as proteases and protons, into the cytosol, resulting in cell death. Salvianolic acid B (Sal B), a water-soluble compound extracted from Salvia miltiorrhiza, exerts a cell protective effect by anti-oxidation. In the present study, we elucidate that Sal B protects hepatocytes from H2O2/CCl4 -induced injury/death by stabilizing the lysosomal membrane.