Résumé
Objective To investigate the effect of electroacupuncture at Zusanli (ST36) point on the expression of cortical actin-binding protein (cortactin) in smooth muscle cells of rats with irritable bowel syndrome(IBS). Methods Eighty female Sprague-Dawley(SD) rats aged 3 months were randomly divided into 4 groups: normal group, model group, acupoint group and sham-acupoint group, 20 rats in each group. The diarrhea-predominant IBS (IBS-D) rat model was established by high-lactose feeding combined with restraint stress method. Acupoint group was given electroacupuncture at Zusanli point, and sham-acupoint group was given electroacupuncture at external region of 5 mm beside Zusanli point. After treatment, time for the discharge of active carbon through all of the gastrointestinal duct was measured, the contraction of rat proximal colon smooth muscle strips was tested, the expression level of cortactin and the ratio of G/F-actin in the proximal colon were detected by Western blotting method. Results Compared with the normal group, time for the discharge of active carbon through all of the gastrointestinal duct was shortened, and the systolic basic tension of colonic smooth muscle, the expression level of cortactin, and the ratio of G/F-actin in the model group were increased (P<0.05). After electroacupuncture treatment, the time for the discharge of active carbon through all of the gastrointestinal duct in acupoint group was prolonged, and the systolic basic tension of the intestinal smooth muscle, the expression level of cortactin, and ratio of G/F-actin were decreased (P < 0.05 compared with the model group and non-acupoint group). Conclusion Electroacupuncture at Zusanli point can effectively improve the gastrointestinal function of IBS rats and has regulatory effect on the contraction of colonic smooth muscle.
Résumé
Objective To investigate the modulation of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD)expression by pravastatin in pre-eclampsia-like mouse model. Methods C57BL/6J mice were randomly injected with N-nitro-L-arginine methyl ester (L-NAME) as pre-eclampsia-like model group (PE) or saline as normal pregnancy control group(Con)respectively,from gestational the 7th to 18th day.For each group,pravastatin(PE+Pra,Con+Pra group)or saline(PE+N,Con+N Group)was given from the 8th to 18th day of gestation,respectively.Liver and placenta of pregnant mice were collected on gestational day 18.The LCHAD protein expression and mRNA levels of liver and placenta were detected through western blot, immunohistochemistry and real-time quantitative PCR. Results (1) The average arterial pressure of pregnant mice increased gradually from the 8th to 18th day in PE+N group,but decreased in PE+Pra group from gestational 10th day, 24 hour urinary protein levels in PE+N group [(1 494 ± 201) μg] were significantly higher than that in Con+N group[(935±128)μg,P<0.01],and also higher than that in PE+Pra group [(981 ± 116) μg, P<0.01].(2) The results of western blot: the expression of LCHAD was significantly lower in PE+N group(liver:0.64±0.11,placenta:0.48±0.06)than that in Con+N group(liver:1.06±0.10, placenta:0.60±0.10),and lower than that in PE+Pra group(liver: 0.99±0.04,placenta:0.60±0.08;all P<0.01).(3)The results of real-time quantitative PCR:the levels of LCHAD mRNA in liver and placenta in PE+N group (liver: 0.621 ± 0.128, placenta: 0.646 ± 0.129) were significantly decreased compared with Con+N group (liver: 1.007 ± 0.130, placenta: 1.004 ± 0.103; all P<0.01), but there was no significant difference between PE+Pra group (liver: 0.693 ± 0.678, placenta: 0.662 ± 0.183;P>0.05). (4) LCHAD protein was expressed widely and evenly in liver.The expression in placental cytotrophoblast and syncytial trophoblast cells located in outer layer of villous in labyrinth layer was the most. The expression of LCHAD was significantly lower in PE+N group(liver: 0.062±0.016,placenta:0.147±0.018)than that in Con+N group (liver: 0.126 ± 0.013, placenta: 0.183 ± 0.024), and lower than that in PE+Pra group (liver: 0.111 ± 0.017, placenta: 0.174 ± 0.027; all P<0.05). Conclusion Pravastatin could upregulate the LCHAD protein expression of liver and placenta in the pre-eclampsia-like mouse,which may be a mechanism to improve the clinical manifestations of pre-eclampsia.