浙江中西医结合杂志

朱青青,赵淑芬,冯萍萍,汪芝欢,徐燕芳.基于p38丝裂原活化蛋白激酶/核因子-κB信号交互探讨柴芍承气汤对高脂血症型急性胰腺炎大鼠肠黏膜微循环的作用机制[J].浙江中西医结合杂志,2026,36(6):

基于p38丝裂原活化蛋白激酶/核因子-κB信号交互探讨柴芍承气汤对高脂血症型急性胰腺炎大鼠肠黏膜微循环的作用机制

Exploring the Mechanism of Chai Shao Cheng Qi Tang on Intestinal Mucosal Microcirculation in Hyperlipidemic Acute Pancreatitis Rats via p38MAPK/NF-κB Signaling Interaction

投稿时间：2025-05-29 修订日期：2026-05-14

DOI：

中文关键词: 高脂血症型急性胰腺炎 p38MAPK/NF-κB 柴芍承气汤

英文关键词:Chai-Shao-Cheng-Qi Decoction Hyperlipidemic acute pancreatitis p38MAPK NF-κB Intestinal microcirculation

基金项目:杭州市科技计划引导项目(20211231Y177),浙江中医药大学附属医院科研项目(2023FSYYZY77),浙江省中医药科技计划项目(2023ZL145)第一作者：朱青青,女,硕士研究生,主治中医师,E-mail:342592401@qq.com通讯作者：徐燕芳,女,主任中医师,从事胰腺炎、慢性萎缩性胃炎等,E-mail：173124831@qq.com ,赵淑芬1^,冯萍萍1^,汪芝欢1^,徐燕芳1^*

作者	单位	E-mail
朱青青	杭州市临安区中医院	342592401@qq.com
赵淑芬
冯萍萍
汪芝欢
徐燕芳^*	杭州市临安区中医院	173124831@qq.com

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中文摘要:

摘要：目的探究柴芍承气汤治疗高脂血症型急性胰腺炎（HLAP）肠黏膜微循环的作用机制。方法取清洁级雄性成年SD大鼠24只，适应性喂养7 d后随机分组为空白对照组、HLAP模型组、柴芍承气汤治疗组，每组8只。用新鲜配制的10% 四丁酚醇（Tyloxapol）溶液诱导大鼠高脂血症模型，以50 μg/kg的诱导剂量腹腔注射20% L-精氨酸（2.5 g/kg）2次（中间间隔1 h）诱导胰腺炎，空白对照组腹腔注射等量生理盐水。造模成功后，柴芍承气汤治疗组给予12.5 g（kg·d）的试验药物灌胃；空白对照组和HLAP模型组给予蒸馏水8 mL（kg·d）灌胃。各组大鼠予普通饲料喂养，其余时间正常进食水，观察大鼠精神状态。给药后28d，每组8只大鼠分批麻醉后取腹主动脉血并处死大鼠进行解剖，迅速解剖胰腺组织。采用生化分析仪检测血淀粉酶(AMY)、三酰甘油（TG），酶联免疫吸附测定法测量炎症因子白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）水平；实时荧光定量聚合酶链式反应（qPCR）法检测各组胰腺组织p38丝裂原活化蛋白激酶（p38 MAPK）和核因子-κB p65（NF-κB p65）基因表达水平；蛋白质免疫印迹法（Western blot）测定胰腺组织NF-κB p65和p38 MAPK磷酸化蛋白表达水平；苏木精-伊红（HE）染色观察胰腺组织病理情况。结果与空白对照组相比，HLAP模型组大鼠血清TG[（504.91±50.89）mmol/L比（11.41±1.22）mmol/L，P<0.01]、AMY[（2583.75±511.74）U/L比（1036.75±536.37）U/L，P<0.01]、IL-6[（37.78±1.61）pg/mL比（33.32±2.49）pg/mL，P<0.05]、TNF-α[（303.54±9.75）pg/mL比（247.44±8.40）pg/mL，P<0.01]和IFN-γ[（2119.85±175.07）pg/mL比（1725.79±78.17）pg/mL，P<0.01]水平均显著升高；胰腺组织中p38 MAPK mRNA[（14.22±2.93）比（1.15±0.64），P<0.01]、NF-κB p65 mRNA[（9.77±1.57）比（1.22±0.64），P<0.01]表达水平显著升高，磷酸化p38 MAPK（p-p38 MAPK）[（1.56±0.35）比（0.07±0.04），P<0.05]和磷酸化NF-κB p65（p-NF-κB p65）[（2.39±0.31）比（0.17±0.07），P<0.05]蛋白表达水平显著升高。与HLAP模型组比较，柴芍承气汤治疗组大鼠TG[（57.60±68.45）mmol/L比（504.91±50.89）mmol/L，P<0.01]、AMY[（1849.04±455.71）U/L比（2583.75±511.74）U/L，P<0.05]、IL-6[（33.78±2.56）pg/mL比（37.78±1.61）pg/mL，P<0.05]、TNF-α[（265.90±13.67）pg/mL比（303.54±9.75）pg/mL，P<0.01]和IFN-γ[（1754.08±70.41）pg/mL比（2119.85±175.07）pg/mL，P<0.01]水平显著降低；胰腺组织中p38 MAPK mRNA[（4.85±0.80）比（14.22±2.93），P<0.01]、NF-κB p65 mRNA[（2.73±0.83）比（9.77±1.57），P<0.01]表达水平显著降低，p-p38 MAPK[（0.08±0.04）比（1.56±0.35），P<0.01]和p-NF-κB p65[（0.19±0.06）比（2.39±0.31），P<0.01]蛋白表达水平显著降低。组织病理学观察显示，HLAP模型组大鼠胰腺腺泡结构紊乱伴炎症浸润，柴芍承气汤治疗组病理损伤明显改善。结论柴芍承气汤通过调控p38 MAPK/NF-κB信号通路相关蛋白表达，抑制下游炎症因子释放，缓解HLAP大鼠胰腺组织明显出血、坏死、水肿及大量炎性细胞浸润等病理改变。

英文摘要:

ABSTRACT: OBJECTIVE Abstract: To investigate the mechanism of Chai-Shao-Cheng-Qi Decoction (CSCQD) in improving intestinal mucosal microcirculation in hyperlipidemic acute pancreatitis (HLAP) by regulating the p38 mitogen-activated protein kinase (MAPK)/nuclear factor-κB (NF-κB) signaling pathway. Methods Twenty-four clean-grade male SD rats were adaptively fed for 7 days and randomly divided into three groups (n=8 per group): blank control, HLAP model, and CSCQD treatment. The HLAP model was induced by intraperitoneal injection of 10% tyloxapol (2.5 g/kg) followed by two doses of L-arginine (50 μg/kg, 1 h apart). The blank control group received saline. After successful modeling, the treatment group was administered CSCQD (12.5 g/kg/day) by gavage, while the other groups received distilled water (8 mL/kg/day). After 28 days, blood samples were collected to measure serum amylase (AMY), triglycerides (TG), and inflammatory cytokines [interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ)] via ELISA. Pancreatic tissues were analyzed for p38 MAPK and NF-κB p65 mRNA expression using qPCR, and protein phosphorylation levels were assessed via Western blot. Histopathological changes were observed using hematoxylin-eosin (HE) staining.Results Compared with the blank control group, rats in the HLAP model group exhibited significantly elevated serum triglyceride levels [504.91 ± 50.89 mmol/L versus 11.41 ± 1.22 mmol/L, P < 0.01] and AMY [2583.75 ± 511.74 U/L versus 1036.75 ± 536.37 U/L, P < 0.01], IL-6 [(37.78 ± 1.61) pg/mL vs. (33.32 ± 2.49) pg/mL, P < 0.05], TNF-α [(303.54 ± 9.75) pg/mL vs. (247.44 ± 8.40) pg/mL, P<0.01], and IFN-γ [2119.85±175.07 pg/mL vs. 1725.79±78.17 pg/mL, P<0.01] were significantly elevated; In pancreatic tissue, p38 MAPK mRNA expression [14.22 ± 2.93 vs. 1.15 ± 0.64, P < 0.01] and NF-κB p65 mRNA expression levels [9.77 ± 1.57 vs. 1.22 ± 0.64, P < 0.01] were significantly elevated in pancreatic tissue. Phosphorylated p38 MAPK (p-p38 MAPK) [(1.56±0.35) vs (0.07±0.04), P<0.05] and phosphorylated NF-κB p65 (p-NF-κB p65) [(2.39±0.31) vs (0.17±0.07), P<0.05]. Compared with the HLAP model group, rats in the CSCQD treatment group exhibited significantly reduced levels of TG [(57.60 ± 68.45) mmol/L vs. (504.91 ± 50.89) mmol/L, P < 0.01], AMY [1849.04 ± 455.71 U/L versus 2583.75 ± 511.74 U/L, P < 0.05], IL-6 [(33.78 ± 2.56) pg/mL vs. (37.78 ± 1.61) pg/mL, P < 0.05], TNF-α [(265.90 ± 13.67) pg/mL vs. (303.54 ± 9.75) pg/mL, P<0.01], and IFN-γ [（1754.08±70.41）pg/mL versus （2119.85±175.07）pg/mL, P<0.01] levels were significantly reduced; In pancreatic tissue, p38 MAPK mRNA expression levels were significantly reduced [(4.85±0.80) vs (14.22±2.93), P<0.01], as were NF-κB p65 mRNA expression levels [(2.73±0.83) vs (9.77±1.57), P<0.01]. p-p38 MAPK [0.08 ± 0.04 vs. 1.56 ± 0.35, P < 0.01] and p-NF-κB p65 [0.19 ± 0.06 vs. 2.39 ± 0.31, P < 0.01] protein expression levels were significantly reduced. Histopathological examination revealed disrupted pancreatic acinar architecture with inflammatory infiltration in the HLAP model group, whereas the CSCQD treatment group demonstrated markedly improved pathological damage. Conclusion CSCQD alleviated pathological changes such as obvious hemorrhage, necrosis, edema and massive inflammatory cell infiltration in pancreatic tissues of HLAP rats by regulating the expression of proteins related to the p38 MAPK/NF-κB signaling pathway and inhibiting the release of downstream inflammatory factors.

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