Electroacupuncture ameliorates corticotrophin-releasing factor-induced jejunal dysmotility in a rat model of stress.

BACKGROUND: Central injection of corticotrophin-releasing factor (CRF) mimics the effect of stress on gastrointestinal (GI) responses, including inhibition of GI motility. This study was designed to explore the effects of electroacupuncture (EA) on disordered jejunal motility in a rat model of stress induced by intracisternal (IC) injection of CRF. METHODS: A stress model was established by IC injection of CRF in Sprague-Dawley rats. GI motility was evaluated by assessing gastric emptying (GE), gastrointestinal transit (GIT) and jejunal motility in vivo. EA was performed at ST36. The functional roles of CRF receptor subtype 1 and subtype 2 (CRFr1 and CRFr2) were examined by IC administration of the corresponding selective CRF antagonists. Protein expression of CRFr1 and CRFr2 in the hypothalamus and jejunum was detected by Western blotting. RESULTS: IC injection of CRF significantly inhibited GE, GIT and jejunal motility. EA treatment remarkably improved the disturbed GI motility. Intriguingly, the disordered jejunal motility induced by central CRF was abolished by IC injection of a selective CRFr2 antagonist, indicating the essential role of central CRFr2 in mediating the stress-induced jejunal motor disorder. EA at ST36 decreased central and peripheral expression of CRFr2, which might be one of the potential mechanisms underlying the beneficial effect of EA on jejunal dysmotility in this rat model of stress. CONCLUSION: This study suggested that EA at ST36 could ameliorate disordered jejunal motility induced by stress, and that this might be associated with the down-regulation of CRFr2.

Peripheral and spinal mechanisms of acupoint sensitization phenomenon.

This study was carried out on adult female Sprague-Dawley rats to observe the position, size, and sensitivity change of inflammatory reactions on body surfaces induced by colorectal import of inflammatory irritant mustard oil. Colorectal distension (CRD) was adopted as a visceral noxious stimulus to record the activities of spinal dorsal horn wide-dynamic range (WDR) neurons activities at spinal segments L1-L3. The study also observed the activations of WDR neurons by electro-acupuncture (EA) on acupoints of Zusanli-Shangjuxu before and after different intensities of CRD stimulation and the dose-response relationship between stimulus and response. The results show that in the case of visceral inflammation, the number of exudation points of neurogenic reaction on body surfaces increased along with the severity of visceral inflammation (Li et al. 2006). The area of peripheral receptive fields of WDR neurons also enlarged along with the intensity of visceral inflammatory response. The activation effect of EA on WDR neurons was positively correlated with the severity of visceral inflammation. Therefore, we concluded that the function of acupoints can be sensitized by visceral noxious stimuli. When the function of internal organs was damaged, the number of reaction points on body surfaces, the size of acupoints' receptive fields, and the sensitivity of acupoints changed accordingly.

[Effects of acupoint-embedment of medicated-thread and acupoint-injection on expression of cortical urokinase-type plasminogen activator and plasminogen activator inhibitor-1 in rats with cerebral ischemia-reperfusion injury].

OBJECTIVE: To observe the effect of acupoint-embedement of medicated-thread and acupoint-injection of Chuanxiongzine on the expression of urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) in the cerebral cortex in rats with cerebral ischemia-reperfusion injury (CI/RI), so as to explore its underlying mechanism in protecting the ischemic cerebral tissue. METHODS: Seventy-eight SD rats were randomly divided into normal control group (n=6), sham operation (sham) group (n=18), model group (n=18),acupoint injection (Al) group (n=18), and acupoint-thread-embedment (ATE) group (n=18). Rats of the latter 4 groups were randomized into 1 d, 3 d and 5 d subgroups, with 6 rats in each. CI/RI model was established by occlusion of the right middle cerebral artery (MCAO) for 30 min and reperfusion. For rats of the Al group, Chuanxiongzine (0.1 mL/200 g) was injected into "Baihui" (GV 20) and "Dazhui" (GV 14), and for those of ATE group, a piece of medicated thread containing collagen protein (extracted from the rat's tail tissue) and Chuanxiongzine + retarder was embedded into GV 20 and GV 14, respectively. The expression of uPA and PAI-1 in the cerebral cortex on the ischemia side was detected by immunohistochemistry. RESULTS: In comparison with the normal control group, the expression of uPA of the ischemia cerebral cortex on day 1, 3 and day 5 in the model group was increased significantly (P < 0.01), while the PAI-1 expression decreased remarkably in the model group (P < 0.01). Compared with the 3 time-points of the model group, cortical uPA expression levels at the 3 time-points in the Al group and those of day 3 and day 5 in the ATE group were down-regulated significantly (P < 0.01), whereas cortical PAI-1 expression levels at the 3 time-points in both AI and ATE groups up-regulated considerably (P < 0.05, P < 0.01). Comparison between AI and ATE groups showed that the expression levels of cortical uPA in the latter group on day 3 and day 5 were significantly lower than those of the former group (P < 0.05), whereas the cortical PAI-1 expression levels in the latter group on day 3 and day 5 were evidently higher than those of the former group (P < 0.05). But, cortical PAI-1 expression of the ATE group on day 1 was significantly lower than that of the AI group (P < 0.05). No significant differences were found between the AI and ATE groups in the expression level of cortical uPA on day 1 and between normal and sham groups in both uPA and PAI-1 expression levels at the 3 time-points (P > 0.05). CONCLUSION: Both AI and ATE can down-regulate cortical uPA expression and up-regulate cortical PAI-1 expression in rats with CI/RI, which may contribute to their protective effect in reducing cerebral ischemic injury.