[Effect of the small needle knife through the Zusanli(ST 36) on behavior and hippocampal expression of NLRP3 and IL-1β in myalgia comorbid depressed rats].

Objective: To observe the effect of the small needle knife through the Zusanli(ST 36) on behavior and hippocampal expression of NLRP3 and IL-1β in myalgia comorbid depressed rats.

Methods: The rat models of myalgia comorbid depression were prepared by intraperitoneal injection of acute reserpine. Twenty-four SD male rats were randomly divided into control group, model group, small needle knife group and amitriptyline group, 6 rats in each group. The open field behavior and mechanical pain threshold of each group were detected. The thermal pain threshold was detected by intelligent hot plate test. The expression of NLRP3 and IL-1β in hippocampus of rats was detected by Western blotting.

Results: Compared with the model group, the mechanical pain threshold of the foot was significantly improved in the small needle knife group (<0.01). Compared with the amitriptyline group, the small needle knife stimulation of Zusanli(ST 36) can significantly increase the thermal pain threshold in rats(<0.05); in the comparison of the horizontal movement distance and the number of crossings in the open field behavioral rats, the total distance of the open field activity of the small needle knife group was significantly increased(<0.05). Compared with the model group, the number of crossings in the small needle knife group had no statistically significant difference (>0.05). The expressions of NLRP3 and IL-1β in the hippocampus of the model group were significantly increased(<0.05), and the expression of IL-1β in the small needle knife group was significantly decreased (<0.05). The stimulation of small needle knife at Zusanli(ST 36) could inhibit the expression of NLRP3 in hippocampus of rats. However, there was no statistically significant difference compared with the model group (>0.05).

Conclusions: Small needle knife can improve the pathological state of myalgia comorbid depression caused by reserpine in rats. The mechanism may be related to the inhibition of NLRP3 inflammasome and IL-1β expression in central hippocampus.