ABSTRACT
Aim: To explore the therapeutic effects of Dendrobium officinale extract on mice with ulcerative colitis(UC) and its mechanism. Methods: The mice were treated with 4% DSS to induce the UC model. The signs or symptom changes of mice were observed and recorded. Then the scores of disease activity index (DAI) during the days of modeling and drug treatment were also evaluated, and the colon tissues were taken as samples. The samples were used for general and microscopic evaluation, the expression of MPO was detected by Western blot, and the expressions of IFN-γ and TNF-α mRNA were measured by qPCR. Meanwhile, the concentrations of serum IFN-γ, TNF-α in mice were also determined by ELISA. Results: As compared with model group, the colon length of mice treated with Dendrobium officinale extract was longer. The DAI score, histological damage score were reduced (P <0. 05 or P <0. 01); the concentrations of IFN-7 and TNF-α inflammatory cytokines in serum decreased (P < 0. 05); the expressions of IFN-γ mRNA and MPO protein in the colon tissue significantly decreased compared with model group (P < 0. 05). Conclusions: Dendrobium officinale extract could treat DSS-induced UC of BALB/c mice. The anti-UC mechanism of Dendrobium officinale extract can be attributed to its ability to reduce the release of IFN-γ and TNF-α and downregulate the expressions of IFN-γ, TNF-α and MPO, to block the amplification effect of inflammation and to achieve its therapeutic effects.
ABSTRACT
Objective: To explore the inhibitory effects of Dendrobium officinale extract (DOE) on gastric carcinogenesis and its related molecular mechanism. Methods: The rats were randomly divided into normal group, model group, positive drug group, low-dose and high-dose DOE groups. The gastric carcinogenesis model was induced by ig giving 200 mg/kg N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) at doses of 200 mg/kg every 10 days for 3 months. Meanwhile, the rats in the treatment groups were given the corresponding doses of drug while the rats in the control group were given normal saline. At the end of the experiment, the degree of gastric tissue carcinogenesis was calculated by HE staining analysis. The expression levels of EGF, EGFR, Bax, and Bcl-2 mRNA were detected by RT-PCR test in gastric tissue. The levels of EGF and EGFR in plasma were detected by ELISA. Apoptosis was detected by TUNEL assay. Results: Compared with the model group, the high-dose DOE could inhibit the degree of carcinogenesis significantly (P < 0.01). Both high-dose and low-dose DOE could significantly reduce the levels of EGF, EGFR mRNA, and Bcl-2 mRNA, and increase the levels of Bax mRNA in gastric tissue, with statistical significance compared with the model group (P < 0.05, 0.01). In addition, they also reduced the levels of EGF and EGFR in plasma significantly and induced apoptosis. Conclusion: DOE could inhibit the gastric carcinogenesis, which might be related to effects of decreasing the expression of EGF and EGFR mRNA in gastric tissue and EGF and EGFR in plasma and inducing the apoptosis through reducing the expression of Bcl-2 mRNA and increasing Bax mRNA.