槲皮素通过抑制细胞凋亡并维持血-睾屏障完整性缓解雷公藤甲素诱导的小鼠生精功能障碍

BAO Bing-hao; WEN Hao-lang; ZHANG Lei; QIN Zhong-jian; HUANG Hao-nan; CHEN Lu; LIU Bao-xing

doi:10.1007/s11655-025-4229-7

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槲皮素通过抑制细胞凋亡并维持血-睾屏障完整性缓解雷公藤甲素诱导的小鼠生精功能障碍

Original Article | Updated：2026-08-04

- 槲皮素通过抑制细胞凋亡并维持血-睾屏障完整性缓解雷公藤甲素诱导的小鼠生精功能障碍
- Quercetin Alleviates Triptolide-Induced Spermatogenic Dysfunction by Reducing Apoptosis and Preserving Blood-Testis Barrier Integrity in Mice
- 中国结合医学杂志（英文版） 2026年32卷第5期页码：423-430
- Affiliations：
  
  1.Department of Andrology, China-Japan Friendship Hospital, Beijing ( 100029), China
  2.Department of Andrology, National Center for Integrative Medicine, China-Japan Friendship Hospital, Beijing ( 100029), China
  3.Graduate School of Beijing University of Chinese Medicine, Beijing ( 100029), China
- Author bio：
  
  Prof. LIU Bao-xing, E-mail: liubaoxing@zryhyy.com.cn
- Funds：
  
  the National Natural Science Foundation of China(82505577;82274517;81873307)
- DOI：10.1007/s11655-025-4229-7
  中图分类号：
- 录用：2025-06-26，
  
  网络首发：2026-01-15，
  
  纸质出版：2026-05
- Accepted：
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BAO Bing-hao, WEN Hao-lang, ZHANG Lei, 等. 槲皮素通过抑制细胞凋亡并维持血-睾屏障完整性缓解雷公藤甲素诱导的小鼠生精功能障碍[J]. 中国结合医学杂志（英文版）, 2026,32(5):423-430.

BAO Bing-hao, WEN Hao-lang, ZHANG Lei, et al. Quercetin Alleviates Triptolide-Induced Spermatogenic Dysfunction by Reducing Apoptosis and Preserving Blood-Testis Barrier Integrity in Mice[J]. Chinese Journal of Integrative Medicine, 2026, 32(5): 423-430.
BAO Bing-hao, WEN Hao-lang, ZHANG Lei, 等. 槲皮素通过抑制细胞凋亡并维持血-睾屏障完整性缓解雷公藤甲素诱导的小鼠生精功能障碍[J]. 中国结合医学杂志（英文版）, 2026,32(5):423-430. DOI： 10.1007/s11655-025-4229-7.

BAO Bing-hao, WEN Hao-lang, ZHANG Lei, et al. Quercetin Alleviates Triptolide-Induced Spermatogenic Dysfunction by Reducing Apoptosis and Preserving Blood-Testis Barrier Integrity in Mice[J]. Chinese Journal of Integrative Medicine, 2026, 32(5): 423-430. DOI： 10.1007/s11655-025-4229-7.

摘要

目的：

探讨槲皮素（quercetin，QE）对生精功能的改善作用，并通过体内实验阐明其潜在分子机制。

方法：

将30只6–8周龄雄性C57BL/6小鼠采用随机数字法随机分为5组（每组

= 6）：对照组、雷公藤甲素（triptolide，TP）模型组（0.1 mg/kg·d），以及不同剂量槲皮素干预组（25、50和100 mg/kg·d）。除对照组外，其余各组均给予TP诱导生精功能损伤，槲皮素干预组在此基础上同期给予QE。干预持续35天，覆盖1个完整的生精周期，并于第38天处死小鼠。采用H

E染色、TUNEL染色及Western blot检测Bcl-2、Bax和cleaved caspase-9的表达，评价生精细胞的病理损伤及凋亡情况。通过免疫荧光和Western blot检测紧密连接蛋白，包括ZO-1和JAMA，评估血-睾屏障（blood-testis barrier，BTB）完整性。采用Western blot检测PI3K、AKT及p-AKT的表达，观察PI3K/AKT信号通路变化。并结合网络药理学和分子对接模拟预测QE的分子作用机制，并进一步进行实验验证。

结果：

QE处理可显著改善TP诱导的睾丸损伤，增加生精上皮厚度和生精小管直径，并减少生精细胞凋亡（

0.05或

0.01）。QE还可改善BTB关键蛋白ZO-1和JAMA的分布及表达水平（

0.05或

0.01）。网络药理学和分子对接研究提示，QE可能通过影响PI3K-AKT信号通路发挥作用；Western blot结果显示AKT磷酸化水平升高（

0.05或

0.01）。

结论：

QE可通过上调PI3K-AKT信号通路，减轻TP诱导的生精功能障碍，减少生精细胞凋亡，并维持BTB结构完整性。QE可能成为治疗TP诱导生精功能障碍的潜在治疗药物。

Abstract

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 (

=6 per group): control

triptolide (TP) model (0.1 mg/kg per day)

and different doses of quercetin (QE) treatment groups (25

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 (

0.05 or

0.01). QE also improved the distribution and expression of key BTB proteins

including ZO-1 and JAMA (

0.05 or

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 (

0.05 or

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.

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