Objective:?To observe the effects of Long Snake Moxibustion on brown adipose tissue (BAT) thermogenesis in rats with a "Yang-deficiency constitution" and to explore its underlying mechanism for improving this constitution.?Methods:?Fifteen SPF-grade SD rats were randomly divided into a normal group, a model group, and a Long Snake Moxibustion group (5 rats per group). The model and Long Snake Moxibustion groups underwent heat-preference screening and generational breeding to establish the Yang-deficiency constitution model. Following modeling, the Long Snake Moxibustion group received treatment for 15 consecutive days. Measurements included anal temperature, body weight, heat preference, ice-water swimming time, and spontaneous activity count. Serum levels of adrenocorticotropic hormone (ACTH), cortisol (CORT), and corticotropin-releasing hormone (CRH) were detected by enzyme-linked immunosorbent assay (ELISA). Hematoxylin and eosin (HE) staining was used to observe lipid droplet morphology in interscapular BAT. The expression of uncoupling protein 1 (UCP1), PTEN-induced kinase 1 (PINK1), and Parkinson's disease-associated protein (Parkin) in BAT was detected by immunohistochemistry and Western Blot.?Results:?Compared with the normal group, the model group exhibited decreased anal temperature, body weight, ice-water swimming time, and spontaneous activity (P<0.01), increased heat preference (P<0.01), lower levels of ACTH and CRH (P<0.001), a reduction in BAT lipid droplet number with enlarged vacuoles, and downregulated protein expression of UCP1, PINK1, and Parkin in BAT (P<0.01). Compared with the model group, the Long Snake Moxibustion group showed increased anal temperature, body weight, ice-water swimming time, and spontaneous activity after treatment (P<0.01), decreased heat preference (P<0.01), elevated levels of ACTH and CRH (P<0.001), an increase in BAT lipid droplet number with smaller vacuoles, and upregulated protein expression of UCP1, PINK1, and Parkin in BAT (P<0.01).?Conclusion:?Long Snake Moxibustion can improve symptoms and serum hormone levels in rats with a Yang-deficiency constitution. The mechanism may be related to activating the PINK1/Parkin pathway to promote mitophagy, thereby increasing UCP1 expression in BAT and enhancing thermogenesis.