机构地区:[1]Guangxi Medical University, Nanning 530021, P. R. China [2]The First Affiliated Hospital of Guangxi Medical University,Nanning 530021, P. R. China
出 处:《广西医科大学学报》2017年第4期481-485,共5页Journal of Guangxi Medical University
基 金:supported by the National Natural Science Foundation of China(No.81360544)
摘 要:Objective:To investigate the effect of Chaihu Shugan decoction(CSD)on gastric smooth muscle cells(GSMCs)apoptosis in rats with functional dyspepsia(FD).Methods:48Sprague-Dawley(SD)rats were randomly assigned into six groups:a normal control group,a model group,apositive control(domperidone)group and low-,middle-and high-dose CSD groups.A rat model of FD was established by constantly squeezing their tails.The rats were administered CSD(0.16g/mL,0.32g/mL,0.64g/mL)or domperidone(0.3 g/L)via intragastric gavage for four weeks.The gastric emptying rate was detected at 4 weeks post-administration.Apoptosis of GSMCs was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL)staining and the mitochondrial morphology was observed by transmission electron microscopy.The expression of Bcl-2and Bax was measured by immunohistochemistry.Results:FD resulted in marked reduction of gastric emptying rate,severe gastric tissue damage and mitochondria injury,but were reversed by CSD treatment(P<0.05).The apoptosis-induced protein Bax was markedly down-regulated by CSD,whereas the expression of the anti-apoptotic Bcl-2 protein was notably increased(P<0.05).Furthermore,CSD could protect the FD rats against GSMCs apoptosis manifested by a decreased in TUNEL-positive cells(P<0.05).Conclusion:CSD could alleviate GSMCs apoptosis in FD rats,possibly by the modulation of Bcl-2 and Bax expression,and the suppression of mitochondria injury.Objective:To investigate the effect of Chaihu Shugan decoction (CSD) on gastric smooth muscle cells (GSMCs) apoptosis in rats with functional dyspepsia (FD). Methods: 48 Sprague-Dawley (SD) rats were randomly assigned into six groups: a normal control group, a model group, a positive control (domperidone) group and low, middle- and high-dose CSD groups. A rat model of FD was established by constantly squeezing their tails. The rats were administered CSD (0.16 g/mL, 0.32 g/mL, 0.64 g/mL) or domperidone (0. 3 g/L) via intragastric gavage for four weeks. The gastric emptying rate was detected at 4 weeks post-administration. Apoptosis of GSMCs was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and the mitochondrial morphology was observed by transmission electron microscopy. The expression of BcL-2 and Bax was measured by immunohistochemistry. Results:FD resulted in marked reduction of gastric emptying rate, severe gastric tissue damage and mitochondria injury, but were reversed by CSD treatment ( P 〈0.05). The apoptosis-induced protein Bax was markedly down-regulated by CSD, whereas the expression of the anti-apoptotic Bcl-2 protein was notably increased (P 〈0. 05). Furthermore, CSD could protect the FD rats against GSMCs apoptosis manifested by a decreased in TUNEL-positive cells ( P 〈0.05). Conelusion..CSD could alleviate GSMCs apoptosis in FD rats, possibly by the modulation of Bcl-2 and Bax expression, and the suppression of mitochondria injury.
分 类 号:R333.2[医药卫生—人体生理学]
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