Li-ESWT treatment reduces inflammation, oxidative stress, and pain via the PI3K/AKT/FOXO1 pathway in autoimmune prostatitis rat models
Li-ESWT treatment reduces inflammation, oxidative stress, and pain via the PI3K/AKT/FOXO1 pathway in autoimmune prostatitis rat models
复制标题
Li-ESWT 治疗通过 PI3K/AKT/FOXO1 通路减轻自身免疫性前列腺炎大鼠模型中的炎症、氧化应激和疼痛
DOI：
10.1111/andr.13027
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发表时间：
2021-09-08
期刊：
影响因子：
4.5
通讯作者：
Wang, Zhiping
中科院分区：
文献类型：
--
作者：
Feng, Bin;Dong, Zhilong;Wang, Zhiping
背景由于慢性前列腺炎/慢性盆腔疼痛综合征(CP/CPPS)的发病机制和治疗效果欠佳的资料有限，迫切需要开发新的有效的治疗方法。低强度体外冲击波疗法(LI-ESWT)已被报道用于CP/CPPS的治疗。然而，其潜在的机制仍有待阐明。目的探讨体外冲击波碎石(LI-ESWT)治疗慢性阻塞性肺疾病(CP/CPPS)的疗效及机制。材料与方法将人前列腺上皮细胞株RWPE-1按不同处理方法随机分为3组：对照组、脂多糖组和LI-ESWT组(LI-ESWT组)。在LI-ESWT治疗后，检测氧化应激水平。然后，我们通过注射前列腺蛋白匀浆和完全弗氏佐剂建立了实验性自身免疫性前列腺炎(EAP)的大鼠模型。将SD大鼠随机分为对照组、EAP组和LI-ESWT组。用von Frey细丝对大鼠盆腔痛觉过敏进行定量研究。收集各组前列腺组织，进行免疫组织化学、氧化应激和蛋白质印迹分析。结果与EAP组比较，LI-ESWT组大鼠前列腺组织炎症反应减轻，细胞因子(TNF-α、IL-1β、IL-6、COX-2、SP)表达减少(均P<0.05)。同样，与EAP组相比，LI-ESWT组的盆腔疼痛和过敏症状有所减轻(均P<；0.05)。此外，LI-ESWT治疗可分别降低前列腺和RWPE-1细胞中的氧化应激(P均<0.05)。此外，LI-ESWT通过抑制AKT/FOXO1信号通路的磷酸化上调CAT的表达。讨论与结论LI-ESWT可通过PI3K/AKT/FOXO1通路减轻自身免疫性前列腺炎大鼠的炎症、氧化应激和疼痛。提示LI-ESWT为CP/CPPS的治疗提供了一种潜在的治疗选择。
Background Due to limited data on the pathogenesis of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and the suboptimal therapeutic effect, the development of new and effective treatment modalities was needed urgently. Low-intensity extracorporeal shock wave therapy (Li-ESWT) has been reported for the treatment of CP/CPPS. However, the underlying mechanism remains to be elucidated. Objective To interrogated the efficacy and the mechanism of Li-ESWT in the treatment of CP/CPPS. Materials and Methods According to different treatments, RWPE-1 cells (human prostate epithelial cells) were randomly divided into three groups: control group, LPS (lipopolysaccharide) group, or Li-ESWT group (LPS-induced RWPE-1 managed by Li-ESWT). Following the Li-ESWT treatment, the levels of oxidative stress were assayed. We then established a rat model of experimental autoimmune prostatitis (EAP) by injecting prostatic protein homogenate mixed with complete Freund's adjuvant. The Sprague-Dawley rats were randomly divided into the control group, EAP group, or Li-ESWT group. Von Frey Filament was used to quantify pelvic hyperalgesia in the rats. Prostates tissues from each group were collected for immunohistochemistry, oxidation stress, and Western blot analysis. Results Histological analysis showed reduced inflammation and expression of cytokines (TNF-alpha, IL-1 beta, IL-6, COX-2, SP) in prostate tissues from the Li-ESWT group compared with those from the EAP group (all p < 0.05). Similarly, there was reduced pelvic pain and allergic symptoms in the Li-ESWT group compared with the EAP group (all p < 0.05). Besides, Li-ESWT treatment could decrease oxidative stress in the prostate and in RWPE-1 cells, respectively (both p < 0.05). Moreover, the Li-ESWT upregulated the expression of CAT through the inhibition of phosphorylation of AKT/FOXO1 signaling pathway. Discussion and Conclusions Li-ESWT may reduce inflammation, oxidative stress, and pain in rats with autoimmunity-induced prostatitis via the PI3 K/AKT/FOXO1 pathway. It implies that Li-ESWT can present a potential therapeutic option for the treatment of CP/CPPS.