RESUMEN
The efficacy of injecting sclerosing agent next to transverse process of cervical vertebra to induce vertebral artery type of cervical syndrome(CSA)was observed.Twenty rabbits were randomly divided into two groups: the model group and the control group.The rabbits in the model group were injected with sclerosing agent next to transverse process of cervical vertebray,on the contrary,the rabbits in the control group were injected with nothing.Transcranial Doppler(TCD)was used to detect the average speed of blood(Vm),pulsatility index(Pi)and the resistant index(Ri)of the vertebral artery,hematoxylin and eosin(HE)staining was used to observe the morphological changes,and immunohistochemistry was used to detect the expression of α-smooth muscle actin(α-SMA)and matrix metalloproteinase-2(MMP-2).TCD showed increased Pi,Ri and decreased Vm in the model group(P<0.05) compared with the control group.HE staining revealed hyperplasia and hypertrophied smooth muscle cells in the model group(P<0.05).Immunohistochemistry displayed up-regulation of α-SMA and MMP-2 in the model group(P<0.05).It was concluded that injecting sclerosing agent next to transverse process of cervical vertebra induces remodeling of vertebral artery in rabbits,suggesting it is a practical method to establish CSA animal model.
RESUMEN
The effects of Wumeiwan (WMW) on TNF-α, IL-6, IL-8, IL-10 and NF-κBp65 in rats with ulcerative colitis (UC) were investigated, the curative effectiveness of WMW vs salicylazosul-fapyridine (SASP) was compared, and the action mechanism was analyzed. Fifty-Six Spra-gue-Dawley (SD) rats were randomly divided into four groups (n=14 in each group, with equal ratio of male and female): normal control group, model group, SASP group, and WMW group. Except normal control group, the rat UC models in the remaining three groups were established using the method of 2.4-dinitrochlorobenzene (DNCB) immunization and acetic acid local enema. The rats in model group, SASP group, and WMW group were treated with distilled water, SASP, and WMW re-spectively. The changes in the symptoms and signs were observed, and levels of IL-6, IL-8, TNF-α,IL-10 and the expression of NF-κBp65 in the colonic tissues were statistically analyzed. The results showed that the levels of IL-6, IL-8, and TNF-α were significantly increased (P<0.01), while those of IL-10 significantly reduced (P<0.01) after establishment of rat UC models as compared with normal control group. The levels of IL-6, IL-8, and TNF-α were obviously lower, bat the level of IL-10 was obviously higher in WMW and SASP groups than those in model group (P<0.05). The levels of IL-6,IL-8, and TNF-α were lower, while the level of IL-10 was higher in WMW group than in SASP group.NF-κBp65 was expressed negatively or weakly in normal colonic tissues. The positive expression rate of NF-κBp65 in WMW group and SASP group was obviously lower than in model group (P<0.01), and there was significant difference between WMW group and SASP group (P<0.05). It was concluded that rat UC model was established successfully. WMW could up-regulate the expres-sion oflL-10, down-regulate the expression ofTNF-α, IL-6, IL-8, and inhibit the NF-κBp65 activity to adjust immune function, indicating WMW had better curative effects on UC in rats.
RESUMEN
Inflammatory bowel disease is thought to be regulated by the balance between Th1 and Th2 cytokines secreted by T cells, and NF-κB p65 also plays a predominant role in the intestinal inflammation. We evaluated the potency of oxymatrine, one of active components of Sophora Root, in inhibiting the immune responses and inflammation in 2,4,6-trinitrobenzene sulfonic acid(TNBS)-induced colitis. The inflammation was markedly ameliorated in the oxymatrine-treated rats.The level of IL-2 was increased and that of IL-10 was decreased in colon tissue in the rat model,which was reversed by the treatment of oxymatrine. Moreover, the elevated expression of NF-κB p65in colon tissue in the model was also improved by oxymatrine treatment. Our results suggest that oxymatrine might be beneficial for the abnormal immune responses and inflammation by regulating the unbalance of Th1 and Th2 cytokines secretion and inhibiting the expression of NF-κB p65 in colon tissue.