Choi Sun Bok, Bae Gi-Sang, Jo Il-Joo, Seo Seung-Hee, Kim Dong-Goo, Shin Joon-Yeon, Hong Seung-Heon, Choi Byung-Min, Park Sang-Hyun, Song Ho-Joon, Park Sung-Joo
From the *BK21 Plus Team, Professional Graduate School of Oriental Medicine, †Department of Herbology, School of Oriental Medicine, ‡Hanbang Body-Fluid Research Center, §Department of Oriental Pharmacy, College of Pharmacy, ∥Wonkwang Oriental Medicines Research Institute, ¶Vestibulocochlear Research Center, and #Department of Biochemistry, School of Medicine, Wonkwang University, Iksan; and **Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup, South Korea.
Pancreas. 2015 Jan;44(1):31-40. doi: 10.1097/MPA.0000000000000195.
We aimed to evaluate the anti-inflammatory and inhibitory effects of Lithospermum erythrorhizon (LE) on cerulein-induced acute pancreatitis (AP) in a mouse model.
Acute pancreatitis was induced via intraperitoneal injection of cerulein (50 μg/kg) every hour for 6 times. In the LE, water extract (100, 250, or 500 mg/kg) was administered intraperitoneally 1 hour before the first injection of cerulein. Six hours after AP, blood, the pancreas, and the lung were harvested for further examination. In addition, pancreatic acinar cells were isolated using a collagenase method, and then, we investigated the acinar cell viability and cytokine productions.
Treatment with LE reduced pancreatic damage and AP-associated lung injury and attenuated the severity of AP, as evidenced by the reduction in neutrophil infiltration, serum amylase and lipase levels, trypsin activity, and proinflammatory cytokine expression. In addition, treatment with LE inhibited high mobility group box 1 expression in the pancreas during AP. In accordance with in vivo data, LE inhibited the cerulein-induced acinar cell death, cytokine productions, and high-mobility group box 1 expression. Furthermore, LE also inhibited the activation of p38 mitogen-activated protein kinases.
These results suggest that LE plays a protective role during the development of AP by inhibiting the activation of p38.
我们旨在评估紫草(LE)对小鼠模型中雨蛙肽诱导的急性胰腺炎(AP)的抗炎和抑制作用。
通过每小时腹腔注射雨蛙肽(50μg/kg),共注射6次来诱导急性胰腺炎。在LE组中,在首次注射雨蛙肽前1小时腹腔注射水提取物(100、250或500mg/kg)。AP发生6小时后,采集血液、胰腺和肺进行进一步检查。此外,采用胶原酶法分离胰腺腺泡细胞,然后研究腺泡细胞活力和细胞因子产生情况。
LE治疗减轻了胰腺损伤和与AP相关的肺损伤,并减轻了AP的严重程度,这表现为中性粒细胞浸润、血清淀粉酶和脂肪酶水平、胰蛋白酶活性以及促炎细胞因子表达的降低。此外,LE治疗抑制了AP期间胰腺中高迁移率族蛋白B1的表达。与体内数据一致,LE抑制了雨蛙肽诱导的腺泡细胞死亡、细胞因子产生以及高迁移率族蛋白B1的表达。此外,LE还抑制了p38丝裂原活化蛋白激酶的激活。
这些结果表明,LE通过抑制p38的激活在AP的发展过程中发挥保护作用。