Effect of Chaihu Shugan decoction on gastric smooth muscle cell apoptosis in rats with functional dyspepsia

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.