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Updated: Apr 26, 2026

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
Published on: May 10, 2024
Protective Effects of Lithospermum erythrorhizon Against Cerulein-Induced Acute Pancreatitis
Sun Bok Choi1, Gi-Sang Bae, Il-Joo Jo
1From 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.
Objectives:
We aimed to evaluate the anti-inflammatory and inhibitory effects of Lithospermum erythrorhizon (LE) on cerulein-induced acute pancreatitis (AP) in a mouse model.
Methods:
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.
Results:
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.
Conclusions:
These results suggest that LE plays a protective role during the development of AP by inhibiting the activation of p38.
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