[Therapeutic effect of Lingze Tablets on benign prostatic hyperplasia in rats: An exploration based on the VEGFA/TNF/IL-6 signaling pathway].

Abstract

Objective: To explore the mechanism of Lingze Tablets (LZT) acting on BPH in rats based on the VEGFA/TNF/IL-6 signaling pathway.

Methods: We equally randomized 30 SPF SD male rats into five groups, normal control, BPH model control, low-dose LZT, medium-dose LZT and high-dose LZT, and established a BPH model in the latter four groups by induction with non-castrate testosterone propionate. After the modeling, we treated the rats in the normal and model groups by intragastrical administration of physiological saline, and those in the latter three groups with low-, medium-, and high-dose LZT respectively, all for 28 successive days. Then we collected the prostate tissue from the animals for observation of the changes in the prostatic indexes and histomorphology, detected the expressions of the proteins related to the VEGFA/TNF/IL-6 signaling pathway, and compared the data obtained among different groups.

Results: Compared with the normal controls, the rats in the model control group showed significant prostatic hyperplasia, markedly increased prostatic index (［0.84 ± 0.01］ g, P<0.05), thickness of the prostatic epithelia and infiltration of the luminal area, and dramatically up-regulated protein expressions of VEGFA (0.60 ± 0.02, P< 0.05), TNF (0.76 ± 0.02, P< 0.05) and IL-6 (0.64 ± 0.02, P< 0.05). In comparison with the model controls, the rats in the low-, medium- and high-dose LZT groups exhibited significantly decreased prostatic indexes (［0.76 ± 0.02］ g, ［0.58 ± 0.02］ g and ［0.52 0.01］ g, all P< 0.05), improved prostatic histomorphology, and down-regulated expressions of VEGFA (0.45 ± 0.01, 0.35 ± 0.01 and 0.31 ± 0.02, all P< 0.05), TNF (0.45 ± 0.01, 0.33 ± 0.01 and 0.27 ± 0.01, all P< 0.01) and IL-6 (0.44 ± 0.01, 0.36 ± 0.01 and 0.30 ± 0.01, all P< 0.01) in a dose-dependent manner.

Conclusion: LZT produces therapeutic effect on BPH by negatively regulating the VEGFA/TNF/IL-6 signaling pathway, reducing the expression levels of VEGFA, TNF and IL-6 proteins, and regulating cell proliferation, apoptosis and inflammatory response.