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小白菊内酯对急性胰腺炎大鼠全身炎症及肠道损伤的影响
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| 篇名： | 小白菊内酯对急性胰腺炎大鼠全身炎症及肠道损伤的影响 |
| TITLE： | Effects of parthenolide on systemic inflammation and intestinal injury in rats with acute pancreatitis |
| 摘要： | 目的 探讨小白菊内酯（PLT）调节Kelch样环氧氯丙烷相关蛋白1（Keap1）/核转录因子红系2相关因子2（Nrf2）/血红素加氧酶1（HO-1）信号通路对急性胰腺炎（AP）大鼠全身炎症及肠道损伤的影响。方法以胆胰管内注射3.5%牛磺胆酸钠溶液（1mL/kg）的方式建立AP大鼠模型，并将造模成功的大鼠分为AP组、PLT（300µg/kg）组、地塞米松（2mg/kg）组、抑制剂（11mg/kgNrf2抑制剂ML385）组、PLT+抑制剂组（300μg/kgPLT+11mg/kgML385），每组10只；另取10只大鼠作为假手术组。各组大鼠尾静脉/腹腔注射相应药液和（或）生理盐水1次。24h后，检测其血清脂肪酶、淀粉酶、氧化应激指标[超氧化物歧化酶（SOD）、丙二醛（MDA）]及炎症因子[白细胞介素1β（IL-1β）、IL-6和肿瘤坏死因子α（TNF-α）]水平；观察其结肠黏膜、胰腺组织病理学变化，并进行Chiu、Schmidt评分，检测其结肠黏膜组织细胞凋亡情况及Keap1、Nrf2、HO-1蛋白表达情况。结果与假手术组比较，AP组大鼠结肠黏膜、胰腺组织炎症细胞浸润明显，可见细胞脱落或组织坏死且出血严重；血清中脂肪酶、淀粉酶、MDA、IL-1β、IL-6、TNF-α水平，Chiu、Schmidt评分，以及结肠黏膜组织的细胞凋亡率和Keap1蛋白的表达均显著升高或上调，血清SOD水平和结肠黏膜组织中Nrf2、HO-1蛋白的表达均显著降低或下调（P＜0.05）。与AP组比较，PLT组、地塞米松组大鼠上述指标均显著改善，抑制剂组则进一步恶化（P＜0.05）；抑制剂可显著逆转PLT对AP大鼠上述指标的改善作用（P＜0.05）。结论PLT抑制了AP大鼠的炎症反应及氧化应激，减轻了肠道损伤，其机制可能与抑制Keap1蛋白的表达、激活Nrf2/HO-1信号通路有关。 |
| ABSTRACT： | OBJECTIVE To investigate the effects of parthenolide （PLT） on systemic inflammation and intestinal injury in rats with acute pancreatitis （AP） by regulating the Kelch-like epichlorohydrin-associated protein 1 （Keap1）/nuclear factor-erythroid-2 related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway. METHODS AP rat model was established by injecting 3.5% sodium taurine cholate solution （1 mL/kg） into the biliary pancreatic duct， and modeled rats were divided into AP group， PLT （300 µg/kg） group， dexamethasone （2 mg/kg） group， inhibitor （11 mg/kg Nrf2 inhibitor ML385） group， and PLT+inhibitor group （300 µg/kg PLT+11 mg/kg ML385）， with 10 rats in each group. Another 10 rats were taken as a sham operation group. Each group was given relevant medicine or normal saline via tail vein/intraperitoneal injection once. After 24 h， serum lipase and amylase levels， the levels of oxidative stress index [superoxide dismutase （SOD） and malondialdehyde （MDA）] and inflammatory factors [interleukin-1β （IL-1β）， IL-6 and tumor necrosis factor-α （TNF-α）] were detected. The histopathological changes in colon mucosa and pancreas were observed， and Chiu and Schmidt scores were performed. The cell apoptosis in colon mucosa and the protein expressions of Keap1， Nrf2 and HO-1 were detected. RESULTS Compared with the sham operation group， there was obvious inflammatory cell infiltration in colon mucosa and pancreatic tissue， cell shedding or tissue necrosis and severe bleeding； serum levels of lipase， amylase， MDA， IL-1β， IL-6 and TNF-α， Chiu and Schmidt scores， apoptotic rate and protein expression of Keap1 in colonic mucosa were significantly increased or up-regulated， while SOD level and protein expressions of Nrf2 20230993） and HO-1 were decreased or down-regulated significantly （P＜0.05）. Compared with the AP group， the above indexes in the PLT group and dexamethasone group were significantly improved， while those in the inhibitor group further deteriorated （P＜0.05）. Inhibitor could significantly reverse the improvement effect of PLT on the above indexes in AP rats （P＜ 0.05）. CONCLUSIONS PLT inhibits inflammation and oxidative stress in AP rats， alleviates intestinal damage， and its mechanism may be related to inhibiting protein expression of Keap1 and activating Nrf2/HO-1 signaling pathway. |
| 期刊： | 2025年第36卷第06期 |
| 作者： | 赵亚男；张蕊；王淑玲；杨春春；王杨；杨明月 |
| AUTHORS： | ZHAO Yanan，ZHANG Rui，WANG Shuling，YANG Chunchun，WANG Yang，YANG Mingyue |
| 关键字： | 小白菊内酯；急性胰腺炎；炎症；肠道损伤；Keap1/Nrf2/HO-1信号通路 |
| KEYWORDS： | parthenolide； acute pancreatitis； inflammation； intestinal injury； Keap1/Nrf2/HO-1 signaling pathway |
| 阅读数： | 3 次 |
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