[Electroacupuncture Intervention Inhibits the Decline of Learning-memory Ability and Overex- pression of Cleaved Caspase-3 and Bax in Hippocampus Induced by Isoflurane in APPswe/PS 1].

OBJECTIVE: To investigate the protection mechanism of electroacupuncture (EA) therapy against Alzheimer's disease (AD)-like neurotoxicity induced by Isoflurane. METHODS: Twenty-four APPswe/PS 1 dE9 double transgenic mice (one of the most extensively used transgenic mouse model of AD) and 24 littermate wild-type mice were randomly assigned into control (Con) group, isoflurane (Iso) group and EA group, respectively (n = 8 in each group). EA (2 Hz/100 Hz, 1 mA) was applied to "Baihui" (GV 20) and "Yongquan" (KI 1) for 15 min, once a day for 3 days. The transgenic mice were exposed to a closed box filled with 1.2% isoflurane + 30% O2 +70% N2 for 4 h. The animals' learning-memory ability was detected by Morris water maze test. The expression of cleaved Caspase-3 in the CA 1 area of hippocampus was detected by immunohistochemistry, and that of hippocampal Bcl-2 and Bax proteins detected by Western blot. RESULTS: Compared with the wilde-type mice, the average escape latency of place navigation test was significantly longer, while the percentage of target-quadrant stay time and the target- platform crossing times of spacial probe test were marked decreased in AD + lso mice (P < 0.05). After acupuncture intervention, the abovementioned changes were reversed (P < 0.05). Correspondingly, compared with the AD-Con group, the number of hippocampal activated Caspase-3-positive cells and the expression of Bax protein were significantly increased in the AD-Iso group (P < 0.05). After EA intervention, the increased Caspase-3-positive cell number and Bax protein expression were remarkably down-regulated in the AD-EA group, and the decreased ratio of Bcl-2/Bax in AD-Iso mice was obviously up-regulated in AD-EA mice (P < 0.05). No significant changes were found in the average escape latency, the percentage of target-quadrant stay time and the target-platofrm corssing times, and inthe number of hippocampal activated Caspase-3-positive cells, the expression levels of hippocampal Bcl-2 and Sax and the ratio of Bcl-2/Bax in the three groups of wilde-type mice (P > 0.05). CONCLUSION: EA intervention can improve the learning-memory ability in AD + Isoflurane mice, suggesting a reduction of AD-like neurotoxicity, which may be associated with its actions in inhibiting the overexpression of activated Caspase-3 and Bax proteins in the hippocampus.

Ginkgo biloba extract (EGb 761) attenuates lung injury induced by intestinal ischemia/reperfusion in rats: roles of oxidative stress and nitric oxide.

AIM: To investigate the effect of ginkgo biloba extract (EGb 761) on lung injury induced by intestinal ischemia/reperfusion (II/R). METHODS: The rat model of II/R injury was produced by clamping the superior mesenteric artery for 60 min followed by reperfusion for 180 min. The rats were randomly allocated into sham, II/R, and EGb + II/R groups. In EGb + II/R group, EGb 761 (100 mg/kg per day) was given via a gastric tube for 7 consecutive days prior to surgery. Rats in II/R and sham groups were treated with equal volumes of the vehicle of EGb 761. Lung injury was assessed by light microscopy, wet-to-dry lung weight ratio (W/D) and pulmonary permeability index (PPI). The levels of malondialdehyde (MDA) and nitrite/nitrate (NO2(-)/NO3(-)), as well as the activities of superoxide dismutase (SOD) and myeloperoxidase (MPO) were examined. Western blot was used to determine the expression of inducible nitric oxide synthase (iNOS). RESULTS: EGb 761 markedly improved mean arterial pressure and attenuated lung injury, manifested by the improvement of histological changes and significant decreases of pulmonary W/D and PPI (P < 0.05 or 0.01). Moreover, EGb 761 markedly increased SOD activity, reduced MDA levels and MPO activity, and suppressed NO generation accompanied by down-regulation of iNOS expression (P < 0.05 or 0.01). CONCLUSION: The results indicate that EGb 761 has a protective effect on lung injury induced by II/R, which may be related to its antioxidant property and suppressions of neutrophil accumulation and iNOS-induced NO generation. EGb 761 seems to be an effective therapeutic agent for critically ill patients with respiratory failure related to II/R.