Objective:To investigate effect of Chaiqin Chengqi Decoction(柴芩承气汤,CQCQD) on changes of neuronal acetylcholine receptor alpha 7(nAChRα7) of peritoneal macrophages in acute pancreatitis(AP).Methods:Eighteen Kunming mice were equally randomized into the control group,AP group and CQCQD treatment group.AP was induced by two intraperitoneal injections of 4 g/kg L-arginine at 1 h apart,while control mice received saline injections.At 72 h after the first injection of L-arginine,mice in the treatment group were intragastrically administered 0.1 mL/10 g CQCQD every 2 h for 3 times,whilst mice in the other two groups received the same amount of saline feeding.Mice were sacrificed by cervical dislocation 2 h after the last feeding of either CQCQD or saline.Peritoneal macrophages were collected for determination of nAChRα7 mRNA and protein expression.Serum was collected for detection of interleukin-6(IL-6),IL-10 and acetylcholine(ACh)levels,and pancreas was for histopathology analysis.Results:The CQCQD treatment significantly ameliorated the severity of AP as evidenced by reducing the pancreatic histopathology score(4.5 ± 0.5 vs.6.2 ± 1.7,P<0.05)and the serum IL-6 levels(1228.31419.2 pg/mL vs.1589.6 ±337.3 pg/mL,P<0.05).The mRNA and protein expression of nAChRα7 of the peritoneal macrophages in the AP group were similar to the control group(P>0.05),but were significantly up-regulated after the CQCQD treatment(P<0.05).The serum ACh levels in the AP group were significantly lower than those in the control group(3.1 ± 0.6 μg/mL vs 4.8 ± 0.7 μg/mL P<0.05),but were significantly increased after the CQCQD treatment(5.6±1.5 μg/mL vs 3.1 ±0.6 μg/mL,P<0.05).Conclusion:CQCQD is protective against L-arginine-induced AP through mechanisms involving nAChR α 7 of peritoneal macrophages.
Objective:To investigate the effect of Chaiqinchengqi decoction(CQCQD) on serum amyloid A (SAA) in severe acute pancreatitis(SAP) patients.Methods:Thirty-five participants enrolled and were randomly assigned into either a treatment condition(n=17,treated with CQCQD) or a control condition(n=18,treated with placebo) 24 hours following the onset of the disease. No statistical difference was observed in either group at baseline.Upon admission,the Acute Physiology and Chronic Health Evaluation scoreⅡ(APACHEⅡ),SAA,serum C-reactive protein (CRP) and interleukin-6(IL-6) were measured,as well as on the first,3rd and 7lh day and were compared between the two groups.Organ complications,infection,operation rate,mortality and hospital stay were also compared.Results:The duration of acute respiratory distress syndrome, acute hepatitis,acute renal failure,gastrointestinal failure and blood coagulation dysfunction were shorter in the treatment group than in those in the control group(P<0.05).The secondary infection rates and the hospital fees in the treatment group were lower than those in the control group(P<0.05) as well as length of hospital stay(P<0.01).After 3 days of hospitalization,the APACHEⅡ,score SAA levels,serum CRP and IL-6 in the treatment group was lower than those in the control group(P<0.05).SAA was positively correlated with serum CRP(R = 0.346,P = 0.042),Ranson score(R = 0.442,P = 0.008) and serum IL-6(R=0.359,P =0.034).The area under the receiver operating characteristic curve of admission SAA predict pancreatic necrosis(PN) was 0.815(95%CI:0.625-0.954;P =0.006).The best cut-off value of admission SAA was 7.85 mg/L with the sensitivity 84.6%and specificity 68.2%.Conclusions:The CQCQD can reduce the duration of organ damage through lowering the SAA in SAP patients and the SAA can early predict the PN and severity of SAP patients.
OBJECTIVE: To explore the effect and the mechanism of Chaiqinchengqi decoction(CQCQD) on the apoptosis-necrosis switch of pancreatic acinar cells in acute necrotizing pancreatitis(ANP) in rats.METHODS: Sixty Sprague-Dawley rats were randomized into the control group, the ANP group and the CQCQD group. The acute pancreatitis(AP)model was induced by intraperitoneal injections of4 g/kg 8% L-Arginine(PH 7.0) twice with a 1 h interval. Rats in the CQCQD group were intragastrically administered CQCQD(20 mL/kg every 2 h, 3 times,then 20 mL/kg every 6 h, 3 times). Rats were killed at the 6 and 24 h after the induction of AP.The pancreatic tissues were collected for pathology and to isolate pancreatic acinar cells and mitochondria.RESULTS: CQCQD significantly ameliorated the severity of ANP by reducing the pancreatic histopathology score, indicated by lactate dehydrogenase levels at the 6 and 24 h. The CQCQD group promoted the apoptosis of pancreatic acinar cells by raising the apoptosis index compared with the ANP group and the control group. Mitochondrial cytochrome c at the 6 and 24 h in the ANP group were lower than that in the control group or the CQCQD group(0.67±0.13 vs 1.54±0.03 vs 0.81±0.09; 0.71±0.08 vs 1.55±0.09 vs 0.89±0.16, P<0.01). The cytochrome c levels in the cytoplasm at the 6 and 2 h in the CQCQD group were higher than in the control group(1.36±0.15 vs 0.67±0.04, 1.46±0.08 vs 0.59±0.09, P<0.01), or the ANP group(0.96±0.13, P>0.05;0.97±0.09, P<0.05). CQCQD increased caspase-3 activity over the ANP group at the 6 h.CONCLUSION: CQCQD can induce apoptosis and relieve the necrosis of pancreatic acinar cells via promoting the release of mitochondrial cytochrome c and increasing pancreatic caspase-3 activity in ANP rats.
Objective:To investigate the effect of Chaiqin Chengqi Decoction(柴芩承气汤,CQCQD)on cholecystokinin receptor 1(CCKRI)-mediated signal transduction of pancreatic acinar cell in rats with acute necrotic pancreatitis(ANP).Methods:Twenty-seven Sprague-Dawley rats were randomized into three groups:the control group,the ANP group,and the CQCQD group(9 in each group).ANP rats were induced by two intraperitoneal injections of 8%L-arginine(pH=7.0,4.4 g/kg) over a 2-h period.Rats were treated with 1.5 mL/100 g body weight of CQCQD(CQCQD group) or physiological saline(control and ANP groups) at 2 h interval.And 6 h after induction,pancreatic tissues were collected for histopathological examination.Pancreatic acinar cells were isolated for determination of CCKR1 mRNA and protein expression,phospholipase C(PLC) and inositol-1,4,5-triphosphate(IP3),and determination of fluorescence intensity(Fl)as a measure of intracellular calcium ion concentration[Ca^(2+)]_i.Results:The pancreatic histopathological score(6.2 + 1.1) and the levels of PLC(1,187.2 ±228.2 μg/mL) and IP3(872.2 ±88.4 μg/mL) of acinar cells in the ANP group were higher than those in the control(2.8 ±0.4,682.5 ±121.8 μg/mL,518.4 ±115.8 μg/mL)and the CQCQD(3.8 ±0.8,905.3 ±78.5 μg/mL,611.0 ±42.5 μg/mL) groups(P<0.05).[Ca^(2+)]_i Fl for the ANP group(34.8 ±27.0) was higher than that in the control(5.1 ±2.2) and CQCQD(12.6 ±2.5) groups(P<0.05).The expression of pancreatic acinar cell CCKR1 mRNA in the ANP group was up-regulated(expression ratio=1.761;P=0.024) compared with the control group.The expression of pancreatic acinar cell CCKR1 mRNA in the CQCQD group was down-regulated(expression ratio=0.311;P=0.035) compared with the ANP group.The ratio of gray values of the CCKR1 and B-actin in the ANP group(1.43 ±0.17) was higher than those in the control(0.70 ±0.15) and CQCQD(0.79 ±0.11) groups(P<0.05).Conclusions:Pancreatic acinar cell calcium overload of ANP induced by L-arginine was related to the up-regulated expressions of pancreatic acinar c
