Seo Sang-Wan, Jung Won-Seok, Lee Sung-Eon, Choi Chang-Min, Shin Byung-Chul, Kim Eun-Kyung, Kwon Kang-Beom, Hong Seung-Heon, Yun Ki-Jung, Park Rae-Kil, Shin Min-Kyo, Song Ho-Joon, Park Sung-Joo
Department of Herbology, College of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 570-749, South Korea.
Pancreas. 2008 Mar;36(2):e22-9. doi: 10.1097/MPA.0b013e31815a396b.
Bee venom (BV) has frequently been used as a remedy for inflammatory diseases. The aim of this study was to investigate the effect of BV on cholecystokinin octapeptide (CCK-8)-induced acute pancreatitis (AP) in rats.
The BV pretreatment group: 0.25 mg/kg BV was administered subcutaneously, followed by 75 mug/kg CCK-8 subcutaneously 3 times after 1, 3, and 5 hours. This whole procedure was repeated for 5 days.
CCK-8 subcutaneously 3 times after 1, 3, and 5 hours for 5 days. The BV posttreatment group: CCK-8 subcutaneously 3 times at an interval of 2 hours for 3 days, and then 0.25 mg/kg of BV was administered subcutaneously.
CCK-8 subcutaneously 3 times at an interval of 2 hours for 3 days.
The BV pretreatment and posttreatment ameliorated many of the examined laboratory parameters (the pancreatic weight [PW]/body weight [BW] ratio, the serum amylase and lipase activity) and reduced histological damages in pancreas. Furthermore, BV pretreatment reduced the production of tumor necrosis factor-alpha, interleukin 1, and interleukin 6 and also decreased pancreatic nuclearfactor-kappaB binding activity compared with saline-treated group in the AP model. The BV also increased heat shock protein 60 (HSP60) and heat shock protein 72 (HSP72) compared with the saline-treated group in the AP model.
These findings suggest that the anti-inflammatory effect of BV in CCK-8-induced AP seems to be mediated by inhibiting nuclear factor-kappaB binding activity, and that BV may have a protective effect against AP.
蜂毒(BV)常被用作治疗炎症性疾病的药物。本研究旨在探讨BV对大鼠胆囊收缩素八肽(CCK-8)诱导的急性胰腺炎(AP)的影响。
BV预处理组:皮下注射0.25mg/kg BV,然后在1、3和5小时后皮下注射75μg/kg CCK-8,共3次。整个过程重复5天。
在1、3和5小时后皮下注射CCK-8,共3次,持续5天。BV后处理组:每隔2小时皮下注射CCK-8,共3天,然后皮下注射0.25mg/kg BV。
每隔2小时皮下注射CCK-8,共3天。
BV预处理和后处理改善了许多检测的实验室参数(胰腺重量[PW]/体重[BW]比值、血清淀粉酶和脂肪酶活性),并减少了胰腺的组织学损伤。此外,与AP模型中的生理盐水处理组相比,BV预处理降低了肿瘤坏死因子-α、白细胞介素1和白细胞介素6的产生,还降低了胰腺核因子-κB结合活性。在AP模型中,与生理盐水处理组相比,BV还增加了热休克蛋白60(HSP60)和热休克蛋白72(HSP72)。
这些发现表明,BV在CCK-8诱导的AP中的抗炎作用似乎是通过抑制核因子-κB结合活性介导的,并且BV可能对AP具有保护作用。