Heavy moxibustion at Sanyin point ameliorates neurogenic bladder dysfunction in spinal cord injury rats through the PI3†K/mTOR pathway.

OBJECTIVE: The present study aims to investigate the effect and mechanism of heavy moxibustion (100 moxa-cone) at Sanyin point (the common point of Yin and kidney) on the function of neurogenic bladder (NB) dysfunction in rats with spinal cord injury (SCI). METHODS: Twenty-four male Sprague-Dawley rats were divided into four groups (n = 6): control, NB, NB + Moxibustion, and NB + Moxibustion + YS-49 (PI3†K agonist). The rats in control groups accepted a cut open of the skin, fascia, and muscle. The NB model was established using spinal cord transection. Fourteen days later, animals received heavy moxibustion at Sanyin point for three weeks or/and intraperitoneal administration of YS-49 (a PI3†K agonist). Basso, Beattie, and Bresnahan (BBB) scale, urodynamic parameters, bladder size, and weight were measured. The hematoxylin-eosin staining method was used to observe the histology of the bladder mucosa. Moreover, NB dysfunction after SCI could be restored by autophagy activation and autophagy is mediated by the PI3†K/Akt/mTOR pathway. Therefore, the expressions of autophagy factor (LC3 II/I and p62), PI3†K, and p-mTOR in the bladder mucosa were evaluated by western blotting. RESULTS: Heavy moxibustion treatment relieved the development of NB dysfunction in rats with SCI, with an increase in the bladder voiding efficiency and a decrease in afferent activity during storage in the moxibustion group compared with the NB group. The expression levels of LC3 II/I were markedly elevated by moxibustion, accompanied by a decrease in the levels of p62. YS-49 addition increased the PI3†K and p-mTOR expression which were down-regulated by moxibustion. Importantly, YS-49 reversed the effects of moxibustion on autophagy and bladder function. CONCLUSION: Heavy moxibustion at Sanyin point exerted its effect on healing-impaired NB dysfunction in rats with SCI, possibly activating autophagy through the PI3†K/mTOR pathway.