[Protective effect of Ligustri Lucidi Ait Polysaccharide against lipopolysaccharide-induced inflammatory injury of Sertoli cells in rats].

OBJECTIVE: To explore the effect of Ligustri Lucidi Ait Polysaccharide (LLP) on lipopolysaccharide (LPS)-induced inflammatory injury of Sertoli cells. METHODS: Rat Sertoli cells were isolated and cultured in vitro and then divided into five groups, blank control, LPS, LPS + low-dose LLP, LPS + medium-dose LLP, and LPS + high-dose LLP. After 48 hours of treatment, the proliferation of the cells was detected by CCK-8, their apoptosis determined by FMC, and the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activity and malondialdehyde (MDA) in the supernatant of the cell culture medium measured by ultraviolet spectrophotometry. The contents of IL-1α, IL-6 and TGF-ß in the culture medium were detected by ELISA before and after removal of LPS. RESULTS: The proliferation of the cells showed statistically significant differences among different groups (F = 153.93, P < 0.01), markedly reduced in the LPS group as compared with the blank control (P < 0.01), but remarkably increased in the high- and medium-dose LLP groups in comparison with the LPS group (both P < 0.01), and so did the apoptosis of the cells (F = 64.06, P < 0.01), significantly increased in the LPS group as compared with the blank control (P < 0.05), but markedly decreased in the high- and medium-dose LLP groups in comparison with the LPS group (both P < 0.01). Statistically significant differences were also observed among different groups in the levels of SOD (F = 56.07, P < 0.01), CAT (F = 41.57, P < 0.01), GSH-Px activity (F = 238.46, P < 0.01), and MDA (F = 285.31, P < 0.01), with decreased SOD, CAT and GSH-Px activity (P < 0.01) and increased MDA (P < 0.01) in the LPS group as compared with the control, but elevated SOD and CAT in the high- and medium-dose LLP groups and increased GSH-Px activity and decreased MDA concentration in all the three LLP groups in comparison with the LPS group (P < 0.01). Before the removal of LPS, the contents of IL-1α, IL-6 and TGF-ß in the culture medium were markedly higher in the LPS than in the control group (all P < 0.01), that of IL-1α was increased significantly in the high- and medium-dose LLP groups (P < 0.01 and P < 0.05) while those of IL-6 and TGF-ß showed no statistically significant differences in the three LPS groups as compared with the LLP group (P > 0.05). After the removal of LPS, the contents of IL-1α and IL-6 were remarkably reduced (t = 25.26 and 61.43, P < 0.01) and that of TGF-ß increased (t = －18.16, P < 0.01), even more significantly in the LLP+LPS groups (P < 0.01). CONCLUSIONS: Ligustri Lucidi Ait Polysaccharide plays a protective role in LPS-induced inflammatory injury of Sertoli cells by reducing cell apoptosis and regulating the contents of IL-1α, IL-6 and TGF-ß from Sertoli cells in inflammation.

Tanshinone IIA induces apoptosis and inhibits the proliferation, migration, and invasion of the osteosarcoma MG-63 cell line in vitro.

Tanshinone IIA (Tan IIA) is an active ingredient extracted from the widely used Danshen root (Salvia miltiorrhiza Bunge), a traditional Chinese medicine. Recent studies have indicated that Tan IIA may play important roles in anticancer treatment. However, its effects on the most common primary malignant bone tumor, osteosarcoma (OS), are unknown. Here, we report that Tan IIA may be an efficacious anti-OS drug as it could induce cell apoptosis and inhibit proliferation, migration, and invasion in vitro. Furthermore, we detected possible molecular mechanisms for Tan IIA activity by examining the levels of Bcl-2, Bax expression, and caspase-3, caspase-8, and caspase-9 activities that regulate apoptosis, matrix metalloproteinase (MMP)-2, and MMP-9 involved in regulating migration and invasion. In this study, we find that Tan IIA inhibits proliferation and induces apoptosis in the human OS cell line MG-63 in a time-dependent and dose-dependent manner. In addition, Tan IIA displays inhibitory activity on OS cell migration and invasion. Mechanistic studies have shown that Tan IIA activity is mediated by caspase activation. Tan IIA was also shown to reduce antiapoptotic Bcl-2, MMP-2, and MMP-9 levels, whereas it increased proapoptotic Bax levels. These data suggest that Tan IIA may be a novel, efficient candidate agent for OS treatment.