Related Experiment Video
Updated: Dec 29, 2025
Isolation of Mouse Respiratory Epithelial Cells and Exposure to Experimental Cigarette Smoke at Air Liquid Interface
Published on: February 21, 2011
Trichostatin A alleviated ovarian tissue damage caused by cigarette smoke exposure
Fang Li1, Jingjing Ding1, Yanfei Cong1
1Department of Obstetrics and Gynecology, Shengjing Hospital, China Medical University, Shenyang, 110004, China; Medical Research Center of Shengjing Hospital, China Medical University, Shenyang, 110004, China; Key Laboratory of Research and Application of Animal Model for Environmental and Metabolic Diseases, Liaoning Province, China.
Abstract:
Cigarette smoke (CS) has a negative impact on women's health and fertility. Studies have shown that histone deacetylases 1 and 2 (HDAC1/2) were involved in oocyte development. However, the roles of HDAC1/2 in ovarian toxicity caused by CS exposure and the therapeutic potential of trichostatin A (TSA, a HDAC inhibitor) for ovarian tissue damage have not been investigated. In this study, Female C57BL/6 mice were exposed to CS from six cigarettes mixed with indoor air for 120 min (one cigarette for 20 min) using a whole-body mainstream smoke exposure system twice daily for 30 days. TSA (0.6 mg/kg body weight) was injected intraperitoneally into mice in the Control + TSA group and CS + TSA group every two days for 30 days. We found that exposure to CS resulted in ovarian tissue damage and HDAC1/2 over-expression. TSA alleviated the structural changes of ovarian tissue induced by smoking and prevented the activation of HDAC1/2. Exposure to CS caused autophagy inhibition and pyroptosis activation. TSA treatment restored the expression of autophagy-associated proteins and decreased the levels of pyroptosis-related proteins induced by CS exposure. The TSA effect may be mediated by inhibition of HDAC1/2 involved in autophagy and pyroptosis process.
Insights
Cigarette smoke damages ovarian tissue by altering histone deacetylases 1 and 2 (HDAC1/2). Trichostatin A (TSA) protects against this damage by inhibiting HDAC1/2, restoring autophagy, and reducing pyroptosis.
Area of Science:
- Reproductive Biology
- Toxicology
- Molecular Biology
Background:
- Cigarette smoke (CS) adversely affects female fertility and reproductive health.
- Histone deacetylases 1 and 2 (HDAC1/2) are implicated in oocyte development.
- The specific roles of HDAC1/2 in CS-induced ovarian toxicity and the therapeutic effects of HDAC inhibitors like trichostatin A (TSA) remain unexplored.
Purpose of the Study:
- To investigate the role of HDAC1/2 in cigarette smoke-induced ovarian toxicity.
- To evaluate the therapeutic potential of trichostatin A (TSA) in mitigating CS-induced ovarian damage.
- To elucidate the molecular mechanisms underlying TSA's protective effects, focusing on autophagy and pyroptosis.
Main Methods:
- Female mice were exposed to CS twice daily for 30 days.
- Mice received intraperitoneal injections of TSA (0.6 mg/kg) every two days.
- Ovarian tissues were analyzed for structural changes, HDAC1/2 expression, autophagy markers, and pyroptosis indicators.
Main Results:
- CS exposure led to ovarian tissue damage and increased expression of HDAC1/2.
- TSA treatment alleviated CS-induced structural damage and prevented HDAC1/2 activation.
- CS inhibited autophagy and activated pyroptosis, while TSA treatment reversed these effects.
Conclusions:
- CS exposure causes ovarian toxicity through HDAC1/2 over-expression, autophagy inhibition, and pyroptosis activation.
- TSA demonstrates therapeutic potential by alleviating CS-induced ovarian damage.
- TSA's protective effects are likely mediated by the inhibition of HDAC1/2, impacting autophagy and pyroptosis pathways.
Related Concept Videos
02:07Oogenesis
01:20Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation