Chinese journal of integrative medicine · 2026
Quercetin Alleviates Triptolide-Induced Spermatogenic Dysfunction by Reducing Apoptosis and Preserving Blood-Testis Barrier Integrity in Mice.
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Bao Bing-Hao, Wen Hao-Lang, Zhang Lei, Qin Zhong-Jian, Huang Hao-Nan, Chen Lu, Liu Bao-Xing
Аннотация
OBJECTIVE: To investigate the ameliorative effects of quercetin (QE) on spermatogenic function and elucidate the underlying molecular mechanisms in vivo.
METHODS: Thirty male C57BL/6 mice (6-8 weeks old) were randomly divided into 5 groups using a random number (n=6 per group): control, triptolide (TP) model (0.1 mg/kg per day), and different doses of quercetin (QE) treatment groups (25, 50, and 100 mg/kg per day, intragastrically). Except for controls, all mice received TP to induce spermatogenic impairment, with concurrent QE administration in treatment groups. The intervention lasted 35 days, covering 1 complete spermatogenic cycle, and mice were euthanized on day 38. Histopathological damage and apoptosis in spermatogenic cells were evaluated using hematoxylin and eosin (H&E) staining, TUNEL assay, and Western blot analysis for Bcl-2, Bax, and cleaved caspase-9. Blood-testis barrier (BTB) integrity was assessed by immunofluorescence and Western blot for tight junction proteins, including zonula occludens-1 (ZO-1) and junctional adhesion molecule A (JAMA). The PI3K/AKT signaling pathway was investigated through Western blot analysis of PI3K, AKT, and phosphorylated AKT (p-AKT). Network pharmacology and molecular docking simulations were performed to predict QE's molecular mechanisms, followed by experimental verification.
RESULTS: QE treatment significantly ameliorated TP-induced testicular damage, increased spermatogenic epithelial thickness and spermatogonial tubule diameter, and decreased apoptosis of spermatogenic cells (P<0.05 or P<0.01). QE also improved the distribution and expression of key BTB proteins, including ZO-1 and JAMA (P<0.05 or P<0.01). Network pharmacology and molecular docking studies suggested that QE influences the PI3K-AKT signaling pathway, which was confirmed by increased AKT phosphorylation levels observed in Western blot results (P<0.05 or P<0.01).
CONCLUSIONS: QE can mitigate TP-induced spermatogenic dysfunction, reduce apoptosis of spermatogenic cells, and preserve BTB structural integrity by upregulating the PI3K-AKT signaling pathway. QE may be a potential therapeutic agent for treating TP-induced spermatogenic disorders.
METHODS: Thirty male C57BL/6 mice (6-8 weeks old) were randomly divided into 5 groups using a random number (n=6 per group): control, triptolide (TP) model (0.1 mg/kg per day), and different doses of quercetin (QE) treatment groups (25, 50, and 100 mg/kg per day, intragastrically). Except for controls, all mice received TP to induce spermatogenic impairment, with concurrent QE administration in treatment groups. The intervention lasted 35 days, covering 1 complete spermatogenic cycle, and mice were euthanized on day 38. Histopathological damage and apoptosis in spermatogenic cells were evaluated using hematoxylin and eosin (H&E) staining, TUNEL assay, and Western blot analysis for Bcl-2, Bax, and cleaved caspase-9. Blood-testis barrier (BTB) integrity was assessed by immunofluorescence and Western blot for tight junction proteins, including zonula occludens-1 (ZO-1) and junctional adhesion molecule A (JAMA). The PI3K/AKT signaling pathway was investigated through Western blot analysis of PI3K, AKT, and phosphorylated AKT (p-AKT). Network pharmacology and molecular docking simulations were performed to predict QE's molecular mechanisms, followed by experimental verification.
RESULTS: QE treatment significantly ameliorated TP-induced testicular damage, increased spermatogenic epithelial thickness and spermatogonial tubule diameter, and decreased apoptosis of spermatogenic cells (P<0.05 or P<0.01). QE also improved the distribution and expression of key BTB proteins, including ZO-1 and JAMA (P<0.05 or P<0.01). Network pharmacology and molecular docking studies suggested that QE influences the PI3K-AKT signaling pathway, which was confirmed by increased AKT phosphorylation levels observed in Western blot results (P<0.05 or P<0.01).
CONCLUSIONS: QE can mitigate TP-induced spermatogenic dysfunction, reduce apoptosis of spermatogenic cells, and preserve BTB structural integrity by upregulating the PI3K-AKT signaling pathway. QE may be a potential therapeutic agent for treating TP-induced spermatogenic disorders.