目的 探讨桦褐孔菌水提物（IOAE）改善慢性非细菌性前列腺炎（CNP）大鼠的作用机制。方法 将48只大鼠随机分为对照组、模型组、普适泰(阳性药，40 mg·kg^-1)组和IOAE低、中、高剂量(35、70、140 mg·kg^-1)组，每组8只。除对照组在前列腺两背侧叶分别注射0.9%氯化钠溶液0.1 mL外，其余各组于相同解剖部位注射等体积25%消痔灵注射液制备CNP模型。于术后第8天开始，对照组、模型组给予等体积蒸馏水，其余各组ig给予对应剂量的药物，每天1次，连续30 d。苏木精-伊红（HE）染色观察前列腺组织变化；ELISA法检测血清白细胞介素（IL）-1β和IL-6含量；分光光度法测定超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）含量；实时荧光定量PCR（qRT-PCR）测定前列腺组织中肿瘤坏死因子（TNF）-α、IL-1β、IL-8、前列腺素E2（PGE2）、环氧化酶-2（COX-2）、IL-18、Toll样受体4（TLR4）、核因子（NF）-κB、NLR家族Pyrin结构域蛋白3（NLRP3）、ASC和半胱氨酸蛋白酶-1（Caspase-1）m RNA表达；Western blotting法检测前列腺组织TLR4、p-NF-κB p65/NF-κB p65、NLRP3、Caspase-1和IL-1β蛋白的相对表达水平。结果 与对照组比较，模型组大鼠前列腺组织内有大量炎性细胞浸润，前列腺组织中SOD、CAT和GSH-Px水平显著降低（P<0.01），而MDA水平显著升高（P<0.01）；血清中IL-1β、IL-6水平、前列腺组织中TNF-α、IL-1β、IL-8、PGE2、COX-2、IL-18、TLR4、NF-κB、NLRP3、ASC、Caspase-1 mRNA相对表达水平及TLR4、p-NF-κB p65/NF-κB p65、NLRP3、Caspase-1、IL-1β蛋白相对表达水平升高（P<0.05、0.01）。与模型组相比，经IOAE高剂量干预后上述指标均显著改善（P<0.05、0.01）。结论 IOAE通过抑制炎症反应和氧化应激，从而减轻CNP大鼠前列腺炎症损伤，其作用机制可能与抑制TLR4/NF-κB/NLRP3信号通路有关。

Objective To investigate the mechanism by which Inonotus obliquus aqueous extract（IOAE） mitigates chronic nonbacterial prostatitis（CNP） in rat models. Methods Forty-eight rats were randomly divided into control group, model group, pusaitai(positive drug, 40 mg·kg^-1) group, and IOAE low-, medium-, and high-dose(35, 70, and 140 mg·kg^-1) groups, with eight rats in each group. Except for the control group, which was injected with 0.1 mL of 0.9% sodium chloride solution into the dorsal lobes of the prostate, the other groups were injected with the same volume of 25% Xihuzhiling injection at the same anatomical site to establish the chronic non-bacterial prostatitis（CNP） model. Starting from the 8 th day after the operation, the control group and the model group were given the same volume of distilled water, while the other groups were ig administered the corresponding doses of drugs once a day for 30 consecutive days. Histological changes in prostate tissue were evaluated using hematoxylin-eosin（HE） staining. Serum concentrations of interleukin-1β（IL-1β） and interleukin-6（IL-6） were measured utilizing enzyme-linked immunosorbent assay（ELISA）. The contents of superoxide dismutase（SOD）, malondialdehyde（MDA）, glutathione peroxidase（GSH-Px）, and catalase（CAT） were determined through spectrophotometric analysis. The relative mRNA expression levels of tumor necrosis factor-α（TNF-α）, IL-1β, IL-8, prostaglandin E2（PGE2）, cyclooxygenase-2（COX-2）, interleukin-18（IL-18）, Toll-like receptor 4（TLR4）, nuclear factor kappa B（NF-κB）, NLR family pyrin domain containing 3（NLRP3）, apoptosis-associated speck-like protein containing a CARD（ASC）, and Caspase-1 in prostate tissue were quantified using reverse transcription-quantitative polymerase chain reaction（qRT-PCR）. Furthermore, Western blotting analysis was conducted to evaluate the relative protein expression levels of TLR4, phosphorylated NF-κB p65 relative to total NF-κB p65（p-NF-κB p65/NF-κB p65）, as well as NLRP3, Caspase-1, and IL-1β in prostate tissue. Results Compared with the control group, the model group had a large number of inflammatory cell infiltrations in the prostate tissue, and the levels of SOD, CAT, and GSH-Px in the prostate tissue were significantly decreased（P < 0.01）, while the MDA level was significantly increased（P < 0.01）; the levels of IL-1β and IL-6 in serum, the relative mRNA expression levels of TNF-α, IL-1β, IL-8, PGE2, COX-2, IL-18, TLR4, NF-κB, NLRP3, ASC, and Caspase-1 in prostate tissue, and the relative protein expression levels of TLR4, p-NF-κB p65/NF-κB p65, NLRP3, caspase-1, and IL-1β in prostate tissue were increased（P < 0.05, 0.01）. Compared with the model group, the above indicators were significantly improved after high-dose IOAE intervention（P < 0.05, 0.01）. Conclusion IOAE mitigates prostatic inflammatory injury in CNP rats by attenuating the inflammatory response and oxidative stress, with its mechanism of action potentially linked to the inhibition of the TLR4/NF-κB/NLRP3 signaling pathway.

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山西省中药管理研究项目(2022ZYYC094); 三晋英才计划自然科学和工程技术领域创新团队(SJYC2024497); 山西中医药大学中药化学学科建设经费(2025XKJS-034)