An experimental study of the therapeutic effect of hydrocortisone on acute pancreatitis-associated lung injury.
Cai Du
Abstract
Cai Du
Abstract
Objective To investigate the therapeutic effect and mechanism of Hydrocortisone on acute necrotic pancreatitis(ANP)-associated lung injury. Methods Fifty-four SD rats were randomized into three groups: sham operation (SO) group, ANP group and Hydrocortisone treatment group. The, ANP model was induced by retrograde injection of 5% sodium taurocholate into the bili-pancreatic duct. The animals in the Hydrocortisone-treatment group were given 10 mg/kg Hydrocortisone 10 min after inducing ANP. Rats in the three groups were killed at 3, 6 and 12 hours after induction of the model. The levels of amylase, TNF-α, IL-6, TXB2, 6-Keto-PGF1α, TXB2/6-Keto-PGF1αin plasma, myeloperoxidase (MPO) in the lung, the wet/dry ratio of lung were measured. Histopathological changes of pancreatic and pulmonary tissues were evaluated. Results The levels of amylase, TNF-α, IL-6, TXB2, TXB2/6 Keto PGF1αand pulmonary MPO significantly increased in ANP group compared with those in SO group(P 0. 05). At 6 and 12 h, the wet/dry ratio of lung also significantly increased in ANP group compared with that in SO group(P 0. 01). Compared with ANP group, administration of Hydrocortisone significantly reduced the levels of TNF-α, IL-6, TXB2, TXB2/6-Keto-PGF1α and pulmonary MPO(P 0. 05); the wet/dry ratio of lung also significantly decreased at 6 and 12 h(P 0.01), and the severity of lung injury was decreased. Conclusions Hydrocortisone may exert the therapeutic effect on ANP associated lung injury by decreasing the production of TXA2, TNF-αand IL-6.
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Objective To investigate the therapeutic effect and mechanism of Hydrocortisone on acute necrotic pancreatitis(ANP)-associated lung injury. Methods Fifty-four SD rats were randomized into three groups: sham operation (SO) group, ANP group and Hydrocortisone treatment group. The, ANP model was induced by retrograde injection of 5% sodium taurocholate into the bili-pancreatic duct. The animals in the Hydrocortisone-treatment group were given 10 mg/kg Hydrocortisone 10 min after inducing ANP. Rats in the three groups were killed at 3, 6 and 12 hours after induction of the model. The levels of amylase, TNF-α, IL-6, TXB2, 6-Keto-PGF1α, TXB2/6-Keto-PGF1αin plasma, myeloperoxidase (MPO) in the lung, the wet/dry ratio of lung were measured. Histopathological changes of pancreatic and pulmonary tissues were evaluated. Results The levels of amylase, TNF-α, IL-6, TXB2, TXB2/6 Keto PGF1αand pulmonary MPO significantly increased in ANP group compared with those in SO group(P 0. 05). At 6 and 12 h, the wet/dry ratio of lung also significantly increased in ANP group compared with that in SO group(P 0. 01). Compared with ANP group, administration of Hydrocortisone significantly reduced the levels of TNF-α, IL-6, TXB2, TXB2/6-Keto-PGF1α and pulmonary MPO(P 0. 05); the wet/dry ratio of lung also significantly decreased at 6 and 12 h(P 0.01), and the severity of lung injury was decreased. Conclusions Hydrocortisone may exert the therapeutic effect on ANP associated lung injury by decreasing the production of TXA2, TNF-αand IL-6.
Key concepts: Lung, Internal medicine, Myeloperoxidase, Hydrocortisone, Therapeutic effect, Medicine, Pancreatitis, Acute pancreatitis