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Inflexinol 通过抑制 cerulein 诱导的胰腺炎中的核因子-κB 激活来减轻急性胰腺炎的严重程度。

Inflexinol reduces severity of acute pancreatitis by inhibiting nuclear factor-κB activation in cerulein-induced pancreatitis.

机构信息

Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea.

出版信息

Pancreas. 2013 Mar;42(2):279-84. doi: 10.1097/MPA.0b013e318264993c.

DOI:10.1097/MPA.0b013e318264993c
PMID:22982818
Abstract

OBJECTIVES

To examine the effect of inflexinol on the development of acute pancreatitis (AP) and to investigate the mechanisms responsible for the protective effect against AP.

METHODS

Acute pancreatitis was induced in mice by intraperitoneal injection of cerulein. Inflexinol was administered intraperitoneally 4 times every 6 hours from 1 hour before the first cerulein injection. Serum amylase activity and histology of the pancreas were measured. Determination of pancreatic nuclear factor-κB (NF-κB) p65 expression was conducted by Western blotting and immunohistochemistry to investigate the mechanisms responsible for the inflexinol effects.

RESULTS

Serum amylase activity in the cerulein group was significantly higher than that in the control group (P < 0.05). Pancreatic histology revealed marked inflammatory changes in the cerulein group such as interstitial edema, vacuolization, necrosis, and infiltration of inflammatory cells; and Western blotting and immunohistochemistry showed marked NF-κB p65 expression. Treatment with inflexinol significantly attenuated the inflammatory changes in pancreatic histology at 24, 48, and 72 hours (P < 0.05). Pancreatic NF-κB p65 expression decreased significantly after inflexinol treatment (P < 0.05).

CONCLUSION

Inflexinol reduced the severity of cerulein-induced AP by inhibiting NF-κB activation.

摘要

目的

研究脂多糖诱导肽(inflexinol)对急性胰腺炎(AP)发展的影响,并探讨其对 AP 的保护作用机制。

方法

通过腹腔注射促胰液素诱导小鼠发生急性胰腺炎。脂多糖诱导肽在第一次注射促胰液素前 1 小时开始,每隔 6 小时腹腔注射 4 次。测量血清淀粉酶活性和胰腺组织学变化。通过 Western blot 和免疫组化测定胰腺核因子-κB(NF-κB)p65 的表达,以研究脂多糖诱导肽作用的机制。

结果

与对照组相比,促胰液素组血清淀粉酶活性明显升高(P<0.05)。胰腺组织学显示,促胰液素组存在明显的炎症变化,如间质水肿、空泡化、坏死和炎症细胞浸润;Western blot 和免疫组化显示 NF-κB p65 表达明显增加。脂多糖诱导肽治疗可明显减轻 24、48 和 72 小时时的胰腺组织学炎症变化(P<0.05)。脂多糖诱导肽治疗后,胰腺 NF-κB p65 表达明显降低(P<0.05)。

结论

脂多糖诱导肽通过抑制 NF-κB 激活,减轻了促胰液素诱导的 AP 的严重程度。

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