期刊
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
卷 25, 期 12, 页码 5753-5768出版社
WILEY
DOI: 10.1111/jcmm.16599
关键词
benign prostatic hyperplasia; chronic non‐ bacterial prostatitis; inflammasome; inflammation; Qianliexin capsule
资金
- project of Quancheng '5150' talent introduction and multiplication plan innovative talents [2017017]
- National Key RD Program [2017YFC1702704]
QLX relieved LUTS in CNP and BPH rat models by inhibiting inflammation, with mechanisms including inhibition of inflammasome activation, NF-kappa B activation, oxidant stress, and autophagy.
Qianliexin capsule (QLX) is a standardized traditional Chinese herbal preparation that has long been used to treat chronic non-bacterial prostatitis (CNP) and benign prostatic hyperplasia (BPH). This study investigated the anti-inflammatory activity of QLX in improving lower urinary tract symptoms (LUTS) associated with CNP and BPH. Rat models of CNP and BPH were induced by oestradiol or testosterone (hormonal imbalance) or chemical inflammation (carrageenan). QLX significantly relieved LUTS in CNP and BPH rat model by reducing prostate enlargement, epithelial thickness, pain response time, urine volume and bleeding time, and by improving prostatic blood flow. The expression of the pro-inflammatory cytokines interleukin (IL)-1 beta and tumour necrosis factor (TNF)-alpha, the pro-inflammatory transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B), and inflammasome components (NLRP3, caspase-1 and ASC) in CNP and BPH tissues was reduced by QLX addition. QLX treatment was followed by reduced cellular malondialdehyde and increased superoxide dismutase, catalase and glutathione peroxidase activity, consistent with antioxidant activity. Increases in Beclin-1 expression and the LC3II/I ratio following QLX treatment indicated that autophagy had been induced. QLX relieved LUTS in CNP and BPH rat models by inhibiting inflammation. The underlying mechanisms included inhibition of inflammasome activation, NF-kappa B activation, oxidant stress and autophagy.
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