Emodin has a protective effect in cases of severe acute pancreatitis via inhibition of nuclear factor‑κB activation resulting in antioxidation

Yao,Wei‑Yan; Zhou,Yu‑Fen; Qian,Ai‑Hua; Zhang,Yong‑Ping; Qiao,Min‑Min; Zhai,Zu‑Kang; Yuan,Yao‑Zong; Yang,Song‑Lin

doi:10.3892/mmr.2014.2789

Emodin has a protective effect in cases of severe acute pancreatitis via inhibition of nuclear factor‑κB activation resulting in antioxidation

Authors:
- Wei‑Yan Yao
- Yu‑Fen Zhou
- Ai‑Hua Qian
- Yong‑Ping Zhang
- Min‑Min Qiao
- Zu‑Kang Zhai
- Yao‑Zong Yuan
- Song‑Lin Yang
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Affiliations: Department of Gastroenterology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, P.R. China, Department of Plastic Surgery, Shanghai Sixth People's Hospital, Shanghai Jiaotong University, Shanghai 200233, P.R. China
Published online on: October 27, 2014 https://doi.org/10.3892/mmr.2014.2789
Pages: 1416-1420

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Abstract

Severe acute pancreatitis (SAP) accounts for up to 20% of acute pancreatitis (AP) cases. The absence of effective treatment options has resulted in a high rate of morbidity and mortality. Emodin is a major component of the Chinese herb rhubarb, which has been widely used in the treatment of numerous diseases, including inflammation and cancer. There are a limited number of studies however, that have investigated the effectiveness of emodin in the treatment of SAP. The present study used a rat model of SAP, to investigate the effect and molecular mechanisms of emodin treatment. Administration of emodin was identified to significantly attenuate SAP, as determined by serum amylase analysis and histological assessment of edema, vacuolization, inflammation and necrosis (P<0.01). Furthermore, treatment with emodin markedly inhibited nuclear factor (NF)‑κB DNA‑binding activity (P<0.01) and the serum expression levels of tumor necrosis factor‑α, interleukin (IL)‑6 and IL‑1β (P<0.05). This attenuation was associated with decreased malondialdehyde and increased superoxide dismutase levels in the pancreatic tissues and serum (P<0.05). This study indicated that administration of exogenous emodin had therapeutic effects on the severity of SAP. The mechanism may be due to inhibition of NF‑κB activation resulting in an antioxidation response, which can subsequently suppress the expression of cytokines.

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