Protective effects of Schisandrin B against D-GalN-induced cell apoptosis in human hepatocyte (L02) cells via modulating Bcl-2 and Bax

Abstract

Schisandrin B is a dibenzocyclooctadiene derivative extracted fromSchisandra chinensis (Turcz.) Baill., that exhibits anti-oxidation, anti-inflammation, anti-tumor and hepatoprotective activities. To understand the hepatoprotective mechanism of schisandrin B, this study investigated the efficacy of schisandrin B on L02 cells after treatment with D-GalN. Following pretreatment with 40 μM schisandrin B, L02 cells were stimulated with 40 mM D-GalN. Cell viability, apoptosis, the expression levels of genes associated with apoptosis, and the intracellular oxidative stress indexes were measured. The viability of L02 cells was determined using MTT assay, and the Annexin V-FITC/PI assay kit was utilized for the assessment of apoptosis. The activities of GSH-Px and SOD, the level of MDA were assessed, separately, using relative detection kits. Moreover, RT-PCR as well as Western blot was applied to measure the mRNA and protein expression of Bax and Bcl-2. The results indicated that schisandrin B significantly prevented D-GalN-induced oxidative damage in L02 cells (P<0.05), decreased GSH-Px and SOD activities (P<0.05), increased MDA content (P<0.05). Furthermore, schisandrin B inhibited D-GalN-induced apoptosis in L02 cells (P<0.05), regulated the expression of Bax and Bcl-2 (P<0.05). The results indicated that schisandrin B decreased the D-GalN-induced intracellular oxidative stress indexes generation, and inhibited the down-regulation of Bcl-2 and up-regulation of Bax induced by D-GalN. In conclusion, schisandrin B was shown to exert protective effect against oxidative damage of L02 cells, which, in part, was achieved by regulating the mRNA and protein levels of Bax and Bcl-2.

Schisandrin B promotes hepatic differentiation from human umbilical cord mesenchymal stem cells

“… 20 Studies have reported that Sch B can effectively prevent cell apoptosis, slow down fibrosis progression, induce cytochrome P450 (CYP) enzyme activity, and promote liver regeneration. 21 , 22 , 23 In addition, several studies have demonstrated that Sch B can inhibit the growth of various types of cancers, including lung cancer, cholangiocarcinoma, gastric cancer, melanoma, and glioma, by inducing cell-cycle arrest or apoptosis. 20 Sch B alleviates myocardial ischemia-reperfusion injury, 24 drug-induced hepatotoxicity 25 and nephrotoxicity 26 by reducing oxidative stress and apoptosis.…”

A tumor microenvironment-stimuli responsive nano-prodrug for overcoming gemcitabine chemoresistance by co-delivered miRNA-21 modulator

“…Many miR-21 target genes are closely associated with carcinogenesis and tumor development [20,21]. For example, TPM1 participates in the formation of cytoskeleton structure [22]; PDCD4 inhibits cell growth [23]; phosphatase and tensin homolog (PTEN) inhibits cell migration and proliferation [24]; reversioninducing-cysteinerich protein with kazal motifs (RECK) inhibits tumor invasion and metastasis [25]; Bcl-2 inhibits cell apoptosis [26], and TIMP3 is involved in the induction of cell apoptosis by extracellular signals [27]. Interestingly, previous study also found that miR-21 level correlates with chemosensitivity in advanced pancreatic cancer [28], and miR-21 inhibitor could ameliorate Gem chemosensitivity [29].…”