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 （CCKR1）-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 （FI） as a measure of intracellular calcium ion concentration [Ca2＋]i. Results： The pancreatic histopathological score （6.2± 1.1） and the levels of PLC （1,187.2±228.2μg/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 μ g/mL, 518.4 ± 115.8 μ g/mL） and the CQCQD （3.8± 0.8, 905.3± 78.5 μ g/mL, 611.0±42.5μ g/mL） groups （P〈0.05）. [Ca2＋]i FI 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; ,0=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 β-actin in the ANP group （1.43±0.17） was higher than those in the control （0.70 ± 0.15） and CQCQD （0.79± 0.1
