2020Indian Journal of Experimental BiologyOpen access

Induction of antioxidant mechanisms in lung during experimental pancreatitis in rats

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Abstract

Lung complications are the most common cause of death in patients with acute pancreatitis. In this study, we investigated how induction of mild acute pancreatitis could modify the course of lung inflammation, eventually, induced by a severe acute pancreatitis in rats. A severe and a mild forms of an experimental acute pancreatitis were respectively established by intra-ductal administration of sodium taurocholate to final dose of 50 mg/kg body wt. and intra-peritoneal injection of caerulein to supramaximal dose of 40 mg/kg body wt. We observed reduced levels of thiobarbiturate acid reacting substances when severe pancreatitis was preceded by the induction of mild pancreatitis. Moreover, mRNAs expression of both HSP-70 and Mn-SOD was increased in the lung. By contrast, the level of glutathione was reduced, but no change in the infiltration of neutrophils was observed. Therefore, we conclude that during the course of pancreatitis and its related lung inflammation, the pulmonary cells response involved in the expression of different protective proteins, including HSP-70 and Mn-SOD, which possibly improves the defensive mechanisms against inflammation in lung cells

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Lung complications are the most common cause of death in patients with acute pancreatitis. In this study, we investigated how induction of mild acute pancreatitis could modify the course of lung inflammation, eventually, induced by a severe acute pancreatitis in rats. A severe and a mild forms of an experimental acute pancreatitis were respectively established by intra-ductal administration of sodium taurocholate to final dose of 50 mg/kg body wt. and intra-peritoneal injection of caerulein to supramaximal dose of 40 mg/kg body wt. We observed reduced levels of thiobarbiturate acid reacting substances when severe pancreatitis was preceded by the induction of mild pancreatitis. Moreover, mRNAs expression of both HSP-70 and Mn-SOD was increased in the lung. By contrast, the level of glutathione was reduced, but no change in the infiltration of neutrophils was observed. Therefore, we conclude that during the course of pancreatitis and its related lung inflammation, the pulmonary cells response involved in the expression of different protective proteins, including HSP-70 and Mn-SOD, which possibly improves the defensive mechanisms against inflammation in lung cells

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Available abstract

Lung complications are the most common cause of death in patients with acute pancreatitis. In this study, we investigated how induction of mild acute pancreatitis could modify the course of lung inflammation, eventually, induced by a severe acute pancreatitis in rats. A severe and a mild forms of an experimental acute pancreatitis were respectively established by intra-ductal administration of sodium taurocholate to final dose of 50 mg/kg body wt. and intra-peritoneal injection of caerulein to supramaximal dose of 40 mg/kg body wt. We observed reduced levels of thiobarbiturate acid reacting substances when severe pancreatitis was preceded by the induction of mild pancreatitis. Moreover, mRNAs expression of both HSP-70 and Mn-SOD was increased in the lung. By contrast, the level of glutathione was reduced, but no change in the infiltration of neutrophils was observed. Therefore, we conclude that during the course of pancreatitis and its related lung inflammation, the pulmonary cells response involved in the expression of different protective proteins, including HSP-70 and Mn-SOD, which possibly improves the defensive mechanisms against inflammation in lung cells

Key concepts: Pancreatitis, Acute pancreatitis, Lung, Inflammation, Medicine, Glutathione, Internal medicine, Gastroenterology

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