■啮齿动物模型中的3-NP诱导已被证明可诱导纹状体随后皮质的选择性神经变性(Brouillet,2014).然而,目前尚不清楚是否,在这种神经毒性条件下,以神经炎症和氧化应激为特征,免疫驻留蛋白的基因表达,T细胞受体β亚基(TCR-β),α7烟碱乙酰胆碱受体(α7nAChRs),核因子κB(NF-κB),炎症细胞因子(TNF-α和IL-6),和抗氧化剂(猫和GpX4)得到调节维生素D3(VD)补充中枢神经系统。
■在本研究中,进行实时聚合酶链反应(RT-PCR)以研究相应基因的表达。将雄性C57BL/6小鼠(8-12周)分为四组,组I:对照(盐水);组II:通过i.p(HD)诱导3-NP;组III:维生素D3(VD)和组IV:(HD+VD)(Manjari等人。,2022年)。
■服用500IU/kg/天的VD后,HD小鼠显示免疫受体的基因表达显著降低,TCR-β亚基,核因子κB(NF-κB),炎性细胞因子,和关键的抗氧化剂,随后乙酰胆碱酯酶活性降低。
■通过对抗免疫受体证明了VD在HD中的一种新的神经保护作用,TCR-β基因表达,抗氧化剂标记,和炎性细胞因子。此外,给予VD0-15天的HD小鼠显示胆碱能信号增强,纹状体和皮质中α7nAChRsmRNA和蛋白质表达恢复。
UNASSIGNED: 3-NP induction in rodent models has been shown to induce selective neurodegeneration in the striatum followed by the cortex (Brouillet, 2014). However, it remains unclear whether, under such a neurotoxic condition, characterized by neuroinflammation and oxidative stress, the gene expression of the immune resident protein, T-cell receptor beta subunit (TCR-β), α7 nicotinic acetylcholine receptor (α7 nAChRs), the nuclear factor kappa B (NF-κB), inflammatory cytokines (TNF-α and IL-6), and antioxidants (Cat and GpX4) get modulated on Vitamin D3 (VD) supplementation in the central nervous system.
UNASSIGNED: In the present study, real-time polymerase chain reaction (RT-PCR) was performed to study the expression of respective genes. Male C57BL/6 mice (8-12 weeks) were divided into four groups namely, Group I: Control (saline); Group II: 3-NP induction via i.p (HD); Group III: Vitamin D3 (VD) and Group IV: (HD + VD) (Manjari et al., 2022).
UNASSIGNED: On administration of 500IU/kg/day of VD, HD mice showed a significant reduction in the gene expression of the immune receptor, TCR-β subunit, nuclear factor kappa B (NF-κB), inflammatory cytokines, and key antioxidants, followed by a decrease in the acetylcholinesterase activity.
UNASSIGNED: A novel neuroprotective effect of VD in HD is demonstrated by combating the immune receptor, TCR-β gene expression, antioxidant markers, and inflammatory cytokines. In addition, HD mice on VD administration for 0-15 days showed an enhancement in cholinergic signaling with restoration in α7 nAChRs mRNA and protein expression in the striatum and cortex.