Combinatorial chemistry & high throughput screening · 2026
The Physiological, Biochemical, and Pathological Characteristics of Adenine-Induced Kidney-Yang Deficiency in Rats.
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Wei Rong-Rui, Lin Qing-Yuan, Geng Zhao, Ma Qin-Ge, Liu Wen-Min, Zhong Guo-Yue, Zhou Qing-Gang, Wu Xu-Tao
Аннотация
INTRODUCTION: Kidney-Yang deficiency is a syndrome crucial for understanding the function of traditional Chinese medicine (TCM) in kidney diseases. The model enables us to explore the applications of TCM for treating Kidney-Yang deficiency and provide practical guidance for TCM.
METHODS: The rats were orally administered medication continuously for 21 days. The thymus, spleen, gland, testis, and epididymis were collected, and organ indices were calculated. The pathological sections of the kidney, spleen, and testis were prepared to observe morphological changes.
RESULTS: This study established a validated, reproducible biomarker framework linking adenineinduced renal injury to Kidney-Yang deficiency. High-dose adenine persistently disrupted the hypothalamic-pituitary-target gland axes and suppresses IL-2-mediated immune function, with causal mechanistic links rather than parallel descriptions. The T4, ACTH, GnRH, LH, and FSH gradually approached normal levels after one week. The high-dose adenine group significantly reduced serum IL-2 levels. Medium- and high-dose adenine induced notable kidney, spleen, and testicular pathological changes in rats. These integrated markers provided a scientifically reproducible bridge for defining Kidney-Yang deficiency with modern biomedical endpoints.
DISCUSSION: The Kidney-Yang deficiency model was established by inducing kidney injury in SD rats with adenine. The kidney injury was closely related to Kidney-Yang deficiency syndrome. The Kidney-Yang deficiency model is crucial for studying drug metabolism in the treatment of the syndrome.
CONCLUSIONS: The low-, medium-, and high-dose adenine-induced Kidney-Yang deficiency models in SD rats impact liver/kidney function and immune indicators. Different adenine doses and modeling times affect biochemical indicators and the severity of Kidney-Yang deficiency to varying degrees.
METHODS: The rats were orally administered medication continuously for 21 days. The thymus, spleen, gland, testis, and epididymis were collected, and organ indices were calculated. The pathological sections of the kidney, spleen, and testis were prepared to observe morphological changes.
RESULTS: This study established a validated, reproducible biomarker framework linking adenineinduced renal injury to Kidney-Yang deficiency. High-dose adenine persistently disrupted the hypothalamic-pituitary-target gland axes and suppresses IL-2-mediated immune function, with causal mechanistic links rather than parallel descriptions. The T4, ACTH, GnRH, LH, and FSH gradually approached normal levels after one week. The high-dose adenine group significantly reduced serum IL-2 levels. Medium- and high-dose adenine induced notable kidney, spleen, and testicular pathological changes in rats. These integrated markers provided a scientifically reproducible bridge for defining Kidney-Yang deficiency with modern biomedical endpoints.
DISCUSSION: The Kidney-Yang deficiency model was established by inducing kidney injury in SD rats with adenine. The kidney injury was closely related to Kidney-Yang deficiency syndrome. The Kidney-Yang deficiency model is crucial for studying drug metabolism in the treatment of the syndrome.
CONCLUSIONS: The low-, medium-, and high-dose adenine-induced Kidney-Yang deficiency models in SD rats impact liver/kidney function and immune indicators. Different adenine doses and modeling times affect biochemical indicators and the severity of Kidney-Yang deficiency to varying degrees.