PloS one · 2026
Vitamin D alleviates neurotoxicity induced by propofol anaesthesia in the offspring of mice.
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Solmaz Hüseyin Cihat, Karacaer Feride, Biricik Ebru, Tunay Demet, Can Müge, Kara Samet, Akıllıoğlu Kübra, Polat Sait
Аннотация
BACKGROUND: Maternal propofol can induce neurotoxicity in the developing brain. Vitamin D modulates neurotrophin and neuromediator synthesis, reduces neuroinflammation and neuroapoptosis. The present study examined whether vitamin D could mitigate maternal propofol induced neurotoxicity in the offspring.
METHOD: Twenty pregnant mice were randomly divided into four groups. During the pregnancy, the groups designated as D and PD were given intraperitoneal vitamin D, while the groups labelled as P and C received 1 ml of saline. On the 14th day of pregnancy, groups P and PD received 200 mg kg-1 of propofol intraperitoneally. Newborn mice from the aforementioned groups were included in the study. The hippocampus and the prefrontal cortex were examined by immunohistochemistry at two postnatal ages: 7 and 45 days (PN7 and PN45). A battery of behavioural assessments was conducted using open field and elevated plus maze tests to evaluate potential alterations at PN45.
RESULTS: Vitamin D reduced the expression of inflammatory and apoptotic factors induced by propofol, such as TNF-α (group P versus group PD: 0.79 (0.76-0.81) versus 0.36 (0.34-0.39), %95 CI; p < 0.001), Bax (group P versus group PD: 0.72 (0.69-0.74) versus 0.52 (0.5-0.54), %95 CI; p < 0.001) in the hippocampus in PN7. The administration of vitamin D resulted in enhanced expression of anti-apoptotic and neuroprotective proteins, such as Bcl-2 (group P versus group PD: 0.3 (0.27-0.33) versus 0.55 (0.53-0.57), %95 CI; p < 0.001) in the hippocampus in PN7. These changes also occurred in the hippocampus in PN45 and the prefrontal cortex in PN7 and PN45. No significant differences were identified in the behavioural tests between the groups.
CONCLUSION: Vitamin D treatment during pregnancy could prevent neurotoxicity in the offspring of mice exposed to propofol.
METHOD: Twenty pregnant mice were randomly divided into four groups. During the pregnancy, the groups designated as D and PD were given intraperitoneal vitamin D, while the groups labelled as P and C received 1 ml of saline. On the 14th day of pregnancy, groups P and PD received 200 mg kg-1 of propofol intraperitoneally. Newborn mice from the aforementioned groups were included in the study. The hippocampus and the prefrontal cortex were examined by immunohistochemistry at two postnatal ages: 7 and 45 days (PN7 and PN45). A battery of behavioural assessments was conducted using open field and elevated plus maze tests to evaluate potential alterations at PN45.
RESULTS: Vitamin D reduced the expression of inflammatory and apoptotic factors induced by propofol, such as TNF-α (group P versus group PD: 0.79 (0.76-0.81) versus 0.36 (0.34-0.39), %95 CI; p < 0.001), Bax (group P versus group PD: 0.72 (0.69-0.74) versus 0.52 (0.5-0.54), %95 CI; p < 0.001) in the hippocampus in PN7. The administration of vitamin D resulted in enhanced expression of anti-apoptotic and neuroprotective proteins, such as Bcl-2 (group P versus group PD: 0.3 (0.27-0.33) versus 0.55 (0.53-0.57), %95 CI; p < 0.001) in the hippocampus in PN7. These changes also occurred in the hippocampus in PN45 and the prefrontal cortex in PN7 and PN45. No significant differences were identified in the behavioural tests between the groups.
CONCLUSION: Vitamin D treatment during pregnancy could prevent neurotoxicity in the offspring of mice exposed to propofol.