Zhonghua wei zhong bing ji jiu yi xue · 2015
[Mitigation of the damage of intestinal smooth muscle of rats with multiple organ dysfunction syndrome by Dachengqi decoction through mitochondrial pathway].
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Luo Peng, Xie Mingzheng, Qi Qinghui
Аннотация
OBJECTIVE: To discuss the mechanism of promotion of gastrointestinal motility during multiple organ dysfunction syndrome (MODS) by Dachengqi decoction, by examining the expression of Bcl-2, Bax of mitochondrial pathway, and nuclear factor-ΚB (NF-ΚB) in smooth muscle of the small intestinal in rats.
METHODS: According to the random number table, 100 healthy adult Wistar rats were divided into three groups: control group with 20 rats, model group with 40 rats, and Dachengqi decoction group with 40 rats. Rat model of MODS was reproduced by bacterial peritonitis induced by an injection of 1 mL Escherichia coli suspension (8×10(8) cfu/mL) into peritoneal cavity. The rats in control group were given 1 mL normal saline intraperitoneally. The rats in Dachengqi decoction group were given 10 mL/kg Dachengqi decoction by gavage, twice a day, before inoculation of the bacterial suspension. Twenty-four hours after modelling, rats in all groups were sacrificed by cervical vertebra luxation, and the upper small intestine was harvested to detect the protein expressions of Bcl-2, Bax, and NF-ΚB in smooth muscle tissue using immunohistochemical staining.
RESULTS: In the control group, a large amount of Bcl-2 protein was expressed and it was distributed uniformly in small intestinal smooth muscle. On the other hand, a small amount of Bax and NF-ΚB protein was expressed, and they were also distributed uniformly. Compared with the control group, Bcl-2 protein was distributed only sparsely, and it was scattered in intestinal smooth muscle in blocks in the model group. The expression of Bcl-2 protein was obviously down-regulated [integral optical density (A) value: 7 115.3±1 797.2 vs. 22 085.5±4 892.2, P < 0.05], and this phenomenon was more prominent in circular muscle layer. Bax and NF-ΚB were densely distributed, and their expressions were upgraded obviously [Bax (A value): 33 802.6±5 778.0 vs. 7 984.4±1 804.5, NF-ΚB (A value): 2 465.9±664.8 vs. 1 572.6±256.0, both P < 0.05]. This phenomenon was more outstanding in circular muscle layer. Compared with that of the model group, the expression of Bcl-2 protein was stronger obviously in intestinal smooth muscle in Dachengqi decoction group (A value: 12 458.6±2 491.1 vs. 7 115.3±1 797.2, P < 0.05). The expressions of Bax and NF-ΚB were down-regulated obviously [Bax (A value): 12 529.2±2 018.5 vs. 33 802.6±5 778.0, NF-ΚB (A value): 1 843.1±373.6 vs. 2 465.9±664.8, both P < 0.05], and the change was more obvious in circular muscle layer.
CONCLUSIONS: Dachengqi decoction may promote recovery of gastrointestinal motility through an increase of Bcl-2 expression in nuclear membrane, thus preventing translocation of Bax to mitochondrion, thereby reduces mitochondrial damage in MODS.
METHODS: According to the random number table, 100 healthy adult Wistar rats were divided into three groups: control group with 20 rats, model group with 40 rats, and Dachengqi decoction group with 40 rats. Rat model of MODS was reproduced by bacterial peritonitis induced by an injection of 1 mL Escherichia coli suspension (8×10(8) cfu/mL) into peritoneal cavity. The rats in control group were given 1 mL normal saline intraperitoneally. The rats in Dachengqi decoction group were given 10 mL/kg Dachengqi decoction by gavage, twice a day, before inoculation of the bacterial suspension. Twenty-four hours after modelling, rats in all groups were sacrificed by cervical vertebra luxation, and the upper small intestine was harvested to detect the protein expressions of Bcl-2, Bax, and NF-ΚB in smooth muscle tissue using immunohistochemical staining.
RESULTS: In the control group, a large amount of Bcl-2 protein was expressed and it was distributed uniformly in small intestinal smooth muscle. On the other hand, a small amount of Bax and NF-ΚB protein was expressed, and they were also distributed uniformly. Compared with the control group, Bcl-2 protein was distributed only sparsely, and it was scattered in intestinal smooth muscle in blocks in the model group. The expression of Bcl-2 protein was obviously down-regulated [integral optical density (A) value: 7 115.3±1 797.2 vs. 22 085.5±4 892.2, P < 0.05], and this phenomenon was more prominent in circular muscle layer. Bax and NF-ΚB were densely distributed, and their expressions were upgraded obviously [Bax (A value): 33 802.6±5 778.0 vs. 7 984.4±1 804.5, NF-ΚB (A value): 2 465.9±664.8 vs. 1 572.6±256.0, both P < 0.05]. This phenomenon was more outstanding in circular muscle layer. Compared with that of the model group, the expression of Bcl-2 protein was stronger obviously in intestinal smooth muscle in Dachengqi decoction group (A value: 12 458.6±2 491.1 vs. 7 115.3±1 797.2, P < 0.05). The expressions of Bax and NF-ΚB were down-regulated obviously [Bax (A value): 12 529.2±2 018.5 vs. 33 802.6±5 778.0, NF-ΚB (A value): 1 843.1±373.6 vs. 2 465.9±664.8, both P < 0.05], and the change was more obvious in circular muscle layer.
CONCLUSIONS: Dachengqi decoction may promote recovery of gastrointestinal motility through an increase of Bcl-2 expression in nuclear membrane, thus preventing translocation of Bax to mitochondrion, thereby reduces mitochondrial damage in MODS.