[Effect of moxibustion with deqi on Aß-receptor mediated transport and enzymatic degradation in hippocampus in rats with Alzheimer's disease].

OBJECTIVE: To observe the clinical effect of moxibustion with deqi on Alzheimer's disease (AD) rats, and evaluate its effect on ß-amyloid (Aß) transport and enzymatic degradation proteins, to explore its molecular mechanism for improving cognitive function. METHODS: Sixty SPF-grade male SD rats were randomly divided into a blank group (8 rats), a sham-operation group (8 rats) and a model establishment group (44 rats). The rats in the model establishment group were injected with Aß1-42 at bilateral ventricles to establish AD model. Among the 38 rats with successful model establishment, 8 rats were randomly selected as the model group, and the remaining rats were treated with mild moxibustion at "Dazhui" (GV 14), once a day, 40 min each time, for 28 days. According to whether deqi appeared and the occurrence time of deqi, the rats were divided into a deqi group (12 rats), a delayed deqi group (10 rats) and a non-deqi group (8 rats). After the intervention, the Morris water maze test was applied to evaluate the cognitive function; the HE staining was applied to observe the brain morphology; the Western blot method was applied to measure the protein expression of Aß and its receptor mediated transport [low-density lipoprotein receptor-related protein (LRP) 1, receptor for advanced glycation end products (RAGE), apolipoprotein E (ApoE)] and enzymatic degradation [neprilysin (NEP), insulin degrading enzyme (IDE), endothelin converting enzyme (ECE)-1 and angiotensin converting enzyme (ACE) 2]. RESULTS: Compared with the sham-operation group, in the model group, the escape latency was prolonged (P<0.01), and the times of platform crossing and the ratio of platform quadrant to total time were reduced (P<0.01); the brain tissue was seriously damaged; the expression of hippocampal Aß and RAGE was increased (P<0.01), and the expression of hippocampal LRP1, ApoE, NEP, IDE, ECE-1 and ACE2 was decreased (P<0.01). Compared with the model group, the escape latency was shortened in the deqi group (P<0.05, P<0.01), and the escape latency in the delayed deqi group and the non-deqi group was shortened from Day 2 to Day 5 (P<0.05, P<0.01), and the times of platform crossing and the ratio of platform quadrant to total time were increased in the deqi group and the delayed deqi group (P<0.01, P<0.05); the brain damage in each moxibustion group was reduced, which was smallest in the deqi group, followed by the delayed deqi group and the non-deqi group; the expression of Aß and RAGE was decreased (P<0.01, P<0.05) and the expression of LRP1 and IDE was increased in each moxibustion group (P<0.01, P<0.05); the expression of ApoE was increased in the deqi group and the delayed deqi group (P<0.01, P<0.05); the expression of NEP was increased in deqi group (P<0.05), and the expression of ECE-1 and ACE2 was increased in the deqi group and the delayed deqi group (P<0.05). Compared with the delayed deqi group and the non-deqi group, the escape latency in the deqi group was shortened from Day 3 to Day 5 (P<0.05), and the times of platform crossing and the ratio of platform quadrant to total time were increased (P<0.05, P<0.01). Compared with the non-deqi group, the expression of Aß was reduced (P<0.05), the expression of LRP1 and ApoE was increased in the deqi group (P<0.05). The expression of NEP in the deqi group was higher than that in the delayed deqi group and the non-deqi group (P<0.05). CONCLUSION: Compared with non-deqi, moxibustion with deqi could promote Aß transport and degradation, thereby reducing Aß level in the brain and improving cognitive function for AD rats.

Stroke treatment in rats with tail temperature increase by 40-min moxibustion.

The distant heat induced by suspended moxibustion (SM) for 40 min is confirmed to have a favorable effect in treating diseases such as ischemic brain injury in the clinical setting, but its precise mechanism remains to be explained. Since a similar reaction to the phenomenon of distant heat is found in some transient middle cerebral artery occlusion (tMCAO) rats treated by a 40-min SM session with tail temperature increase (TTI), we hereby study its mechanism by comparing the neuroprotective effect of 40 min's SM with TTI to those without. The experimental results show that 40 min's SM with TTI can significantly reduce the infarct volume and neurological deficit score in tMCAO rats. Western blot demonstrates that a reduction in the levels of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) expression in tMCAO rats with TTI is more striking than that of the rats without TTI. The expression of caspase-3 protein is inhibited in tMCAO rats with TTI. The results suggest that the efficacy of SM for 40 min with TTI is higher than that without. Although neuroprotective effects present in tMCAO rats with and without TTI, those with TTI revealed a higher level of anti-inflammation effect and exhibited an anti-apoptosis effect.