The regulation and the mechanism of melatonin in calcium overload of pancreatic acinar cell / 中华消化杂志

ABSTRACT

Objective To investigate the regulation and the mechanism of Melatonin in calcium overload of pancreatic acinar cell in acute necrotizing pancreatitis (ANP). Methods Fifty-four Sprague-Dawley (SD) rats were equally divided into three groupssham-operation group (SO group),ANP group (created with retrograde cholangiopancreatography injection of sodium taurocholate) and MT group (ANP model made after intra-peritoneal injection MT for 30 mins).Rats were sacrificed at 1,4 and 8hours after operation and pancreas tissues were underwent pathological examination.The free calcium concentration of pancreas tissues was determined by fluorescence minitoring method; and the expression of CaMK Ⅱ in pancreas tissues at mRNA and protein level was tested by real-time PCR and Western Blot.Results Pancreatic pathological injury in ANP groups was progressively severe as time extended,which was obviously ameliorated in MT group compared with ANP group (the t value of compared pathological score at 1,4 and 8 hour was-7.95,-9.72 and -7.69,all P=0.00).Compared at same time point,the free Ca2+ concentration of pancreas tissues in ANP group was significantly higher than that of SO group (the t value of 1,4 and 8 hour was 13.09,18.58 and 16.56,all P=0.00).It was a little bit higher in MT group compared with that of SO group,however was significantly lower than that of ANP group (the t value of 1,4 and 8 hour was -10.03,-11.75 and -11.02,all P =0.00).Compared with SO group,the expression of CaMK Ⅱ at mRNA and protein level significantly increased in ANP group; MT significantly inhibited its expression.Conclusions The expression of CaMK Ⅱ may be inhibited by MT interfere,and then lower the calcium overload in pancreatic acinar cell,which play a role in pancreas tissue protection.