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[Effect of PFT-α on apoptosis of spermatogenic cells caused by enorchia]
Li Xie1, Liping He, Zhiying Yang
1Department of Basic Medicine, Changsha Health Vocational College, Changsha 410100, China.
Objective:
To determine the molecular mechanism of germ cell apoptosis via investigating the effect of PFT-α on the expression of p53 and bcl-2/bax during experimental cryptorchid cell apoptosis.
Methods:
Male Sprague-Dawley rats were assigned into 4 groups: a sham-operated group, a cryptorchid group, a cryptorchid+p53 inhibitor (p53 inhibitor-alpha, PFT-α) group, and a cryptorchid+dissolvent of PFT-α [dimethyl sulphoxide (DMSO)] group. Unilateral cryptorchidism was surgically induced in the rats of the cryptorchid group, PFT-α group, and cryptorchid+dissolvent of PFT-α group. The rats in the PFT-α group and cryptorchid+dissolvent of PFT-α group were intra-peritoneally injected PFT-α and dissolvent of PFT-α, respectively, once a day. The rats were killed on the 7th day after the surgery. The morphology of spermatogenic epithelium at the side of surgery in the rats was observed under light microscope. The apoptosis of spermatogenic cells in the unilateral cryptorchidism was evaluated by TUNEL and flow cytometry (FCM). The protein expression levels of p53, bcl-2, and Bax were detected by Western blot and immunohistochemical assay in turn.
Results:
Compared with the cryptorchid groups and the cryptorchid+dissolvent of PFT-α group, the seminiferous epithelium of the cryptorchid+p53 inhibitor group appeared orderly, with thicker cell layers and lower apoptosis index, weak protein expression level of p53/Bax and strong protein expression level of bcl-2.
Conclusion:
PFT-α inhibits the germ cell apoptosis caused by the experimental cryptorchidism via increasing the expression of bcl-2 and decreasing the expression of p53 and bax.
Insights
PFT-α protects against cryptorchidism-induced germ cell apoptosis by modulating p53 and bcl-2/bax expression. This p53 inhibitor increases bcl-2 and decreases p53 and bax, preserving testicular function.
Area of Science:
- Reproductive Biology
- Molecular Biology
- Cell Biology
Background:
- Experimental cryptorchidism induces germ cell apoptosis, impacting male fertility.
- The molecular mechanisms underlying germ cell apoptosis in cryptorchidism require further elucidation.
- p53 and bcl-2/bax family proteins are key regulators of apoptosis.
Purpose of the Study:
- To investigate the effect of p53 inhibitor-alpha (PFT-α) on germ cell apoptosis in experimental cryptorchidism.
- To determine the impact of PFT-α on the expression of p53, bcl-2, and bax proteins.
- To elucidate the molecular mechanism of PFT-α in preventing germ cell apoptosis.
Main Methods:
- Male Sprague-Dawley rats underwent unilateral cryptorchidism surgery.
- Rats were treated with PFT-α or its dissolvent (DMSO).
- Apoptosis was assessed using TUNEL and flow cytometry; protein expression of p53, bcl-2, and bax was analyzed via Western blot and immunohistochemistry.
Main Results:
- PFT-α treatment significantly reduced germ cell apoptosis in cryptorchid rats.
- The seminiferous epithelium structure was preserved in the PFT-α treated group.
- PFT-α treatment led to decreased expression of p53 and bax, and increased expression of bcl-2.
Conclusions:
- PFT-α effectively inhibits germ cell apoptosis induced by experimental cryptorchidism.
- The protective effect of PFT-α is mediated by the modulation of p53, bax, and bcl-2 protein expression.
- PFT-α represents a potential therapeutic agent for preserving male fertility in cases of cryptorchidism.
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