Molecular biology reports · 2026
Molecular and functional interplay of prostaglandin F2 alpha and oxytocin in camel corpus luteum using in vitro model.
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Hussein Zein, Ibrahim Sally, Mahmoud Karima, Fathi Mohamed, Mohammed Faten F, Ismail Tayseer I M
Аннотация
BACKGROUND: This study investigated the molecular and functional mechanisms of luteolysis in the mature camel corpus luteum (CL) in response to prostaglandin F2 alpha (PGF), oxytocin (OXT), and their combination.
METHODS AND RESULTS: CL from mature she-camel were obtained and in vitro cultured in a modified media, then subjected to hormonal treatments for 24 h, including prostaglandin (PFG; 1000 µM), oxytocin (OXT; 300 IU), or a combination thereof. The collected CL underwent RNA isolation and subsequent qRT-PCR analysis to assess the expression of key luteolytic genes: PTGFR, FASLG, and OXTR. Progesterone (P4) concentrations in the culture media were determined, and histological examinations were performed on the CL tissues. PGF treatment alone induced potent luteolysis, characterized by a significant reduction in P4 concentration (from 18.33 ± 2.85 to 5.44 ± 1.58 ng/mL), severe structural degeneration, and a marked four-fold upregulation of PTGFR and FASLG mRNA transcripts. Furthermore, OXT alone had no significant effect on P4 levels or gene expression. Crucially, the co-administration of PGF and OXT resulted in striking functional-structural dissociation: P4 secretion was maintained at control levels (18.43 ± 4.75 ng/mL), and the PGF-induced upregulation of PTGFR and FASLG was significantly attenuated (two-fold increase).
CONCLUSION: OXT exerts a novel anti-luteolytic effect by interfering with the PGF-mediated molecular cascade, while the combination may simultaneously trigger a rapid, non-apoptotic structural collapse. This dissociation highlights a robust compensatory mechanism in the camel CL and suggests a potential therapeutic strategy for controlled luteal regression in camel breeding programs.
METHODS AND RESULTS: CL from mature she-camel were obtained and in vitro cultured in a modified media, then subjected to hormonal treatments for 24 h, including prostaglandin (PFG; 1000 µM), oxytocin (OXT; 300 IU), or a combination thereof. The collected CL underwent RNA isolation and subsequent qRT-PCR analysis to assess the expression of key luteolytic genes: PTGFR, FASLG, and OXTR. Progesterone (P4) concentrations in the culture media were determined, and histological examinations were performed on the CL tissues. PGF treatment alone induced potent luteolysis, characterized by a significant reduction in P4 concentration (from 18.33 ± 2.85 to 5.44 ± 1.58 ng/mL), severe structural degeneration, and a marked four-fold upregulation of PTGFR and FASLG mRNA transcripts. Furthermore, OXT alone had no significant effect on P4 levels or gene expression. Crucially, the co-administration of PGF and OXT resulted in striking functional-structural dissociation: P4 secretion was maintained at control levels (18.43 ± 4.75 ng/mL), and the PGF-induced upregulation of PTGFR and FASLG was significantly attenuated (two-fold increase).
CONCLUSION: OXT exerts a novel anti-luteolytic effect by interfering with the PGF-mediated molecular cascade, while the combination may simultaneously trigger a rapid, non-apoptotic structural collapse. This dissociation highlights a robust compensatory mechanism in the camel CL and suggests a potential therapeutic strategy for controlled luteal regression in camel breeding programs.