Reproductive toxicity of triptolide and its mechanism in male rats

Huang, Zhengjun; Que, Huiqing; Peng, Hua-yi; Lin, Sen; Guo, Shim-min; Qian, Liping

doi:10.4268/cjcmm20152322

Cited by 4 publications

(1 citation statement)

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“…Carpesii Fructus altered the activities of defense enzymes (SOD, CAT and GSH-Px) in another in vivo study (Xia et al, 2017). Testicular marker enzymes such as LDH, G-6-PD and β-G; testosterone synthetic enzymes including StAR, P450scc, P450c17, 3β-HSD and 17β-HSD; spermatogenic enzymes including SDH, LDH and ACP and estradiol synthesis enzyme aromatase were changed after triptolide and glycosides from Tripterygium wilfordii Hook F (GTW) exposure (Huang et al, 2015;Jing et al, 2017;Ma et al, 2015;Zhang, Huang, et al, 2012). Codeine, a risk compound in Papaver somniferum L., led to testicular enzymes (ALP, ACP, LDH and GGT) variation with chronic administration (Akhigbe & Ajayi, 2020).…”

Section: Enzymesmentioning

confidence: 99%

Risk compounds, potential mechanisms and biomarkers of traditional Chinese medicine‐induced reproductive toxicity

Yan

Zhang

et al. 2022

J of Applied Toxicology

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With the increasing application of traditional Chinese medicine (TCM), TCM-induced reproductive toxicity has gradually aroused people's concern. Various TCM, such as Tripterygium wilfordii Hook. f., Radix Aconiti lateralis Preparata and Rhizoma Pinelliae, are currently reported to cause reproductive toxicity in humans and animals. However, a summary of the material bases, mechanisms and biological markers of TCMinduced reproductive toxicity is still lacking. This review filled the gap by searching and summarising relevant studies and articles published on PubMed, CNKI and Web of Science databases from January 2000 to November 2021. The risk ingredients involved in TCM-induced reproductive toxicity were divided into glycosides, alkaloids, phenols, terpenoids, anthraquinones, lactones, plant toxin proteins, animal toxins and so forth. Potential mechanisms underlying TCM-induced reproductive toxicity, including steroidogenic toxicity, lipids metabolism abnormity, energy insufficiency, oxidative stress and apoptosis, were illustrated. We also outlined possible biomarkers, especially biomarkers of effect involved in TCM-induced reproductive toxicity, including anti-oxidant enzymes, signalling pathways, genes and growth factors.

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Section: Enzymesmentioning

confidence: 99%

Risk compounds, potential mechanisms and biomarkers of traditional Chinese medicine‐induced reproductive toxicity

Yan

Zhang

et al. 2022

J of Applied Toxicology

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WITHDRAWN: Toxicity of triptolide and the molecular mechanisms involved

Chen

Peng

et al. 2017

Environmental Toxicology and Pharmacology

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<p>Ginsenoside Rg3 protects mouse leydig cells against triptolide by downregulation of miR-26a</p>

Liang

Zhang

2019

DDDT

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Background Ginsenoside Rg3 has been reported to exert protection function on germ cells. However, the mechanisms by which Rg3 regulates apoptosis in mouse Leydig cells remain unclear. In addition, triptolide (TP) has been reported to induce infertility in male rats. Thus, this study aimed to investigate the protective effect of Rg3 against TP-induced toxicity in MLTC-1 cells. Methods CCK-8, immunofluorescence assay, Western blotting and flow cytometry were used to detect cell proliferation and cell apoptosis, respectively. In addition, the dual luciferase reporter system assay was used to detect the interaction between miR-26a and GSK3β in MLTC-1 cells. Results TP significantly inhibited the proliferation of MLTC-1 cells, while the inhibitory effect of TP was reversed by Rg3. In addition, TP markedly induced apoptosis in MLTC-1 cells via increasing the expressions of Bax, active caspase 3, Cyto c and active caspase 9, and decreasing the level of Bcl-2. However, Rg3 alleviated TP-induced apoptosis of MLTC-1 cells. Moreover, the level of miR-26a was obviously downregulated by Rg3 treatment. The protective effect of Rg3 against TP-induced toxicity in MLTC-1 cells was abolished by miR-26a upregulation. Meanwhile, dual-luciferase assay showed GSK3β was the direct target of miR-26a in MLTC-1 cells. Overexpression of miR-26a markedly decreased the level of GSK3β. As expected, upregulation of miR-26a could abrogate the protective effects of Rg3 against TP-induced cytotoxicity via inhibiting the expression of GSK3β. Conclusion These results indicated that Rg3 could protect MLTC-1 against TP by downregulation of miR-26a. Therefore, Rg3 might serve as a potential agent for the treatment of male hypogonadism.

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Reproductive toxicity of triptolide and its mechanism in male rats

Cited by 4 publications

References 0 publications

Risk compounds, potential mechanisms and biomarkers of traditional Chinese medicine‐induced reproductive toxicity

Risk compounds, potential mechanisms and biomarkers of traditional Chinese medicine‐induced reproductive toxicity

WITHDRAWN: Toxicity of triptolide and the molecular mechanisms involved

<p>Ginsenoside Rg3 protects mouse leydig cells against triptolide by downregulation of miR-26a</p>

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