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Qianliexin capsule exerts anti‐inflammatory activity in chronic non‐bacterial prostatitis and benign prostatic hyperplasia via NF‐κB and inflammasome

机译:千叶松胶囊在慢性非细菌前列腺炎和良性前列腺增生中施加抗炎活性通过NF-κB和炎症

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摘要

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)‐1β and tumour necrosis factor (TNF)‐α, the pro‐inflammatory transcription factor nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB), 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‐κB activation, oxidant stress and autophagy.
机译:前列欣胶囊(QLX)是长期以来一直用于治疗慢性非细菌性前列腺炎(CNP)和良性前列腺增生(BPH)规范的中国传统中药制剂。本实验研究在改善与CNP和BPH相关的下泌尿道症状(LUTS)QLX的抗炎活性。 CNP和BPH大鼠模型的雌二醇或睾酮(荷尔蒙失调)或化学性炎症(卡拉胶)引起的。 QLX通过降低前列腺肿大,上皮厚度,疼痛反应时间,尿量和出血时间,并通过改善前列腺血流显著减轻在CNP和BPH大鼠模型LUTS。的促炎细胞因子白细胞介素(IL)-1β和肿瘤坏死因子(TNF)-α的表达,所述促炎转录因子核因子激活的B细胞的κ-轻链增强子(NF-κB),和炎性组分(NLRP3,胱天蛋白酶-1和ASC)在CNP和BPH组织中通过QLX加成降低。 QLX治疗随后减少蜂窝丙二醛和增加的超氧化物歧化酶,过氧化氢酶和谷胱甘肽过氧化物酶的活性,具有抗氧化活性是一致的。在的Beclin-1的表达和以下QLX治疗LC3II / I比增加表明自噬已被诱导。 QLX缓解LUTS在CNP和BPH大鼠模型通过抑制炎症。潜在的机制包括炎性活化,NF-κB的活化,氧化应激和自噬的抑制。

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