ArticleJournal of ovarian research2025
Tanshinone IIA alleviates tri-ortho-cresyl phosphate-induced ovarian damage through Hippo signaling pathway activation in mice.
Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
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10 authors.
Funding
Abstract
backgroundTri-ortho-cresyl phosphate (TOCP), a widely used plasticizer, has been shown to impair ovarian function. While tanshinone IIA exhibits ovarian protective effects in aging models, its potential to counteract TOCP-induced ovarian damage and associated signaling mechanisms remains unexplored. This study investigates the therapeutic effects of tanshinone IIA on TOCP-damaged ovaries in mice, with focus on Hippo, AKT, and MAPK pathways.
resultsTOCP exposure (200 mg/kg/d for 28 days) significantly reduced ovarian follicle counts (primordial, preovulatory, and mature follicles) and disrupted hormone levels (elevated Estrogen(E2), decreased Follicle stimulating hormone(FSH)/ Anti-Mueller tube hormone(AMH)) in mice. Treatment with high-dose tanshinone IIA restored ovarian structure and function: growing follicle counts increased significantly (p < 0.001), FSH (p < 0.001) and AMH (p < 0.001) levels surged to marked degrees, while E2 (p < 0.001) levels decreased significantly. All changes were statistically significant. Immunohistochemistry and Western blot analysis revealed that tanshinone IIA restored ovarian AMH and Follicle-Stimulating Hormone Receptor (FSHR) protein expression, which were suppressed by TOCP. In vitro experiments further demonstrated that TOCP dose-dependently inhibited granulosa cell viability (p < 0.001) and proliferation (p < 0.001). Co-treatment with tanshinone IIA (0.01 mM) rescued cell viability (p < 0.01) and proliferation (p < 0.05). Mechanistically, tanshinone IIA suppressed ovarian apoptosis (p < 0.01) and modulated multiple signaling pathways: it attenuated Hippo signaling (p < 0.05) and reactivated PI3K/AKT (p < 0.05), p38 (p < 0.05), and ERK1/2 (p < 0.01) pathways.
conclusionsTanshinone IIA alleviates TOCP-induced ovarian dysfunction primarily through coordinated modulation of Hippo signaling and AKT/MAPK pathway activities, offering a potential therapeutic strategy for chemical-induced ovarian injury.
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