Baicalin ameliorates experimental inflammatory bowel disease through polarization of macrophages to an M2 phenotype.

Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders of the intestinal tract. Baicalin, originally isolated from the root of the Chinese herb Huangqin (Scutellaria baicalensis Georgi) and its main active ingredient, has a protective effect against inflammatory responses in several diseases. The present study investigated the effects of baicalin on macrophage polarization and its therapeutic role in IBD. Murine peritoneal macrophages and mice with colitis were treated with baicalin. Macrophage subset distribution, M1 and M2 macrophage-associated mRNA expression, and interferon regulatory factor 4 and 5 (IRF4 and IRF5) expression were analyzed. siRNA transfection into mouse peritoneal macrophages was utilized to suppress IRF4. Fluorescence-activated cell sorting, western blot, and real-time PCR analyses were performed. Baicalin (50µM) limited lipopolysaccharide (LPS)-induced M1 macrophage polarization; decreased LPS-induced tumor necrosis factor α, interleukin (IL)-23, and IRF5 expression; and increased IL-10, arginase-1 (Arg-1), and IRF4 expression. siRNA-mediated IRF4 silencing significantly impaired baicalin activity. Furthermore, pretreatment with baicalin (100mg/kg) in mice with dextran sodium sulfate (DSS)-induced colitis ameliorated the severity of colitis and significantly decreased the disease activity index (baicalin group, 3.33±0.52 vs. DSS group, 5.67±1.03). Baicalin (100mg/kg) also repressed IRF5 protein expression and promoted IRF4 protein expression in the lamina propria mononuclear cells, and induced macrophage polarization to the M2 phenotype. In summary, our results showed that baicalin upregulates IRF4 protein expression and reverses LPS-induced macrophage subset redistribution. Thus, baicalin alleviates DSS-induced colitis by modulating macrophage polarization to the M2 phenotype.

[Anti-tumor activity of safflower polysaccharide (SPS) and effect on cytotoxicity of CTL cells, NK cells of T739 lung cancer in mice].

OBJECTIVE: To study the anti-tumor activity of SPS in vivo and in vitro and the cytotoxicity of CTL cells, NK cells of T739 lung cancer in mice. METHOD: The transplanted tumor model of S180 Sarcoma was established with KM mouse. The SPS was adminished i.p. for 10 d, the tumor weight was detected. The transplanted tumor model of LA795 lung cancer was established with T739 mouse and SPS was adminished i.p. for 10 d and the tumor weight and the cytotoxicity of CTL cells, NK cells were detected. The Anti-tumor activity of SPS on three types of tumor cells in vitro was observed with trypan blue exclusion staining. RESULT: SPS 40 mg x kg(-1) can significantly inhibit the growth of S180 Sarcoma in mice and inhibitory rate was 51.33% (P<0.01). It can also inhibit the growth of LA795 lung cancer in mice and the tumor volume was reduced obviously for 3.29 mm3 (P<0.05). It can remarkably enhance the cytotoxicity of splenic CTL cells, NK cells in tumor-bearing (P<0.05). CONCLUSION: SPS have anti-tumor effects, the mechanism of the anti-tumor activity may be related to enhance the cytotoxicity of CTL cell and NK cell.