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

Protective effects of Schisandrin B against D-GalN-induced cell apoptosis in human hepatocyte (L02) cells via modulating Bcl-2 and Bax.
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DOI:
10.1080/21655979.2021.1979863
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发表时间:
2021-12
期刊:
影响因子:
4.9
通讯作者:
Wu Z
Wu Z
中科院分区:
生物学2区
文献类型:
--
作者:
Hu Y;Li H;Li R;Tian Y;Wu Z

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五味子乙素B是从五味子中提取的二苯并环辛二烯衍生物。保释其显示出抗氧化、抗炎、抗肿瘤和肝保护活性。为了解五味子乙素B的保肝作用机制,本研究观察了五味子乙素B对D-半乳糖胺处理的L02细胞的作用。在用40 μM五味子素B预处理后,用40 mM D-GalN刺激L02细胞。检测细胞活力、凋亡、凋亡相关基因表达水平和细胞内氧化应激指标。MTT法检测细胞活力,Annexin V-FITC/PI法检测细胞凋亡。采用相应的检测试剂盒分别测定GSH-Px、SOD活性和MDA水平。RT-PCR和Western blot检测Bax和Bcl-2的mRNA和蛋白表达。结果表明,五味子乙素B能显著抑制D-GalN诱导的L02细胞氧化损伤(P<0.05),降低GSH-Px和SOD活性(P<0.05),升高MDA含量(P<0.05)。五味子乙素B能抑制D-半乳糖胺诱导的L02细胞凋亡(P<0.05),并能调节Bax和Bcl-2的表达(P<0.05)。结果表明,五味子乙素B可降低D-GalN诱导的细胞内氧化应激指标的产生,抑制D-GalN诱导的Bcl-2的下调和Bax的上调。结论:五味子乙素B对L02细胞氧化损伤具有保护作用,其机制可能与调节Bax和Bcl-2的mRNA和蛋白水平有关。
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.
DOI: 10.3390/life11020163
发表时间: 2021-02-20
期刊: Life (Basel, Switzerland)
影响因子: --
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