Xiaohong Wang1, Xun Zhuang2, Ronglong Wei3, Chunrong Wang4, Xianglong Xue5, Ling Mao6. 1. Department of Gastroenterology, Danyang People's Hospital, Danyang 212300, JS, China. Electronic address: wx102474wx@163.com. 2. Department of Gastroenterology, Danyang People's Hospital, Danyang 212300, JS, China. Electronic address: zhuangxun33@163.com. 3. Department of Gastroenterology, Danyang People's Hospital, Danyang 212300, JS, China. Electronic address: Weironglong33@163.com. 4. Department of Gastroenterology, Danyang People's Hospital, Danyang 212300, JS, China. Electronic address: Wangchunrong44@163.com. 5. Department of Gastroenterology, Danyang People's Hospital, Danyang 212300, JS, China. Electronic address: Xuexianglong55@163.com. 6. Department of Gastroenterology, Danyang People's Hospital, Danyang 212300, JS, China. Electronic address: Maoling567@163.com.
Abstract
OBJECTIVES: To observe the protecting effects of Acanthopanax and Ulinastatin against severe acute pancreatitis (SAP)-induced brain injury in rats. METHODS: SAP-modeled rats were equally randomized into three groups: model group, Acanthopanax-treated group and Ulinastatin-treated group. A sham-operation group was used as negative control. Serum tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and IL-10 levels were assayed by enzyme linked immunosorbent assay (ELISA). Nuclear factor kappa B p65 (NF-κB p65) activity in the brain tissue was determined by immunohistochemistry. The mortality, pathological changes of the pancreas and brain, and expression of TNF-α mRNA, IL-6 mRNA and IL-10 mRNA in the brain tissue were observed at 6, 12 and 24h after operations in all groups. RESULTS: The mortality of the model group was significantly higher than that of both treatment groups at 24h (P<0.01). Serum levels of TNF-α and IL-6, activity of NF-κB p65, expression levels of TNF-α and IL-6 mRNA in the brain tissue, and the pathological scores of the pancreas and brain in the two treatment groups were lower than those in the model group at 12 and 24h after operation (P<0.01), while serum IL-10 and IL-10 mRNA expression levels of the brain tissue in the two treatment groups were higher. There was no significant difference in all indexes between Acanthopanax and Ulinastatin groups at all designated time points (P>0.05). CONCLUSIONS: Acanthopanax and Ulinastatin have similar protecting effects against SAP-induced brain injury in rats.
OBJECTIVES: To observe the protecting effects of Acanthopanax and Ulinastatin against severe acute pancreatitis (SAP)-induced brain injury in rats. METHODS:SAP-modeled rats were equally randomized into three groups: model group, Acanthopanax-treated group and Ulinastatin-treated group. A sham-operation group was used as negative control. Serum tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and IL-10 levels were assayed by enzyme linked immunosorbent assay (ELISA). Nuclear factor kappa B p65 (NF-κB p65) activity in the brain tissue was determined by immunohistochemistry. The mortality, pathological changes of the pancreas and brain, and expression of TNF-α mRNA, IL-6 mRNA and IL-10 mRNA in the brain tissue were observed at 6, 12 and 24h after operations in all groups. RESULTS: The mortality of the model group was significantly higher than that of both treatment groups at 24h (P<0.01). Serum levels of TNF-α and IL-6, activity of NF-κB p65, expression levels of TNF-α and IL-6 mRNA in the brain tissue, and the pathological scores of the pancreas and brain in the two treatment groups were lower than those in the model group at 12 and 24h after operation (P<0.01), while serum IL-10 and IL-10 mRNA expression levels of the brain tissue in the two treatment groups were higher. There was no significant difference in all indexes between Acanthopanax and Ulinastatin groups at all designated time points (P>0.05). CONCLUSIONS: Acanthopanax and Ulinastatin have similar protecting effects against SAP-induced brain injury in rats.