仙人掌属 humifusa 改善了雨蛙肽诱导的急性胰腺炎。

Opuntia humifusa ameliorated cerulein-induced acute pancreatitis.

机构信息

From the *Department of Herbology, School of Oriental Medicine, †BK21 plus team, Professional graduate school of Oriental medicine, ‡Hanbang Body-fluid Research Center, §College of Pharmacy, and Institute of Pharmaceutical Research and Development, and ∥College of Pharmacy, Wonkwang University, Iksan, Jeonbuk; ¶ChungBuk Technopark Bio Center, Jecheon, #Foundation of industry-academy cooperation, Semyung University, ChungBuk; and **Department of Medicinal Herb, Gyeongju University, Gyeongbuk, South Korea.

出版信息

Pancreas. 2014 Jan;43(1):118-27. doi: 10.1097/MPA.0b013e318296f903.

DOI:10.1097/MPA.0b013e318296f903

PMID:24326366

Abstract

OBJECTIVE

The aim of this study was to evaluate the effects of Opuntia humifusa (OH) on cerulein-induced acute pancreatitis (AP).

METHODS

Acute pancreatitis was induced via intraperitoneal injection of cholecystokinin analog cerulein (50 μg/kg). In the OH pretreatment group, OH was administered intraperitoneally (100, 250, or 500 mg/kg) 1 hour before first cerulein injection. In the posttreatment group, OH was administered intraperitoneally (500 mg/kg) 1 hour after the first cerulein injection. Furthermore, we isolated the pancreatic acinar cells using collagenase method, then investigated the acinar cell viability, cytokine productions, and the regulating mechanisms.

RESULTS

The both pretreatment and posttreatment of OH treatment attenuated the severity of AP, as shown by the histology of the pancreas and lung, and inhibited neutrophil infiltration; serum amylase and lipase activities; proinflammatory cytokine expression such as interleukin 1, interleukin 6, and tumor necrosis factor α; and cell death including apoptosis and necrosis. Furthermore, OH inhibited the activation of c-Jun N-terminal kinases.

CONCLUSIONS

These results suggest that OH reduces the severity of AP by inhibiting acinar cell death through c-Jun N-terminal kinases.

摘要

目的

本研究旨在评估仙人掌（OH）对胆囊收缩素类似物亮肽诱导的急性胰腺炎（AP）的影响。

方法

通过腹腔内注射胆囊收缩素类似物亮肽（50μg/kg）诱导急性胰腺炎。在 OH 预处理组中，在第一次亮肽注射前 1 小时腹腔内给予 OH（100、250 或 500mg/kg）。在治疗组中，在第一次亮肽注射后 1 小时腹腔内给予 OH（500mg/kg）。此外，我们使用胶原酶法分离胰腺腺泡细胞，然后研究腺泡细胞活力、细胞因子产生和调节机制。