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Peak At Science: 2023 January 17

Peak At Science 20230117
Open Access

Peak At Science: 2023 January 17

Insulin ameliorates dim blue light at night-induced apoptosis in hippocampal neurons via the IR/IRS1/AKT/GSK3β/β-catenin signaling pathway

In recent years, the damaging effects of night light pollution, one of the environmental pollutions, on memory has been attracting attention. However, the underlying molecular mechanisms by which light at night, especially blue light at night, impairs memory remains unclear. Here, a total of 42 C57BL6/J mice that exposed to no light at night, dim white light at night (dLAN-WL), or dim blue light at night (dLAN-BL) for 28 days. Behavioral data indicated that exposure to dLAN-BL resulted in severe recognition memory impairment, as evidenced by the reduced recognition index and discrimination index in the novel object recognition test. At the same time, we observed a decrease in plasma insulin levels. Consistent with these changes, we also observed that dLAN-BL reduced the number of neurons in the CA1, CA3 and DG regions of the hippocampus, up-regulated the mRNA expression levels of Bax, down-regulated the mRNA expression levels of Bcl-2, Bcl-xl and the protein expression level of pIRS1, pAKT, pGSK3β, β-catenin in the hippocampus. In vitro experiments, we found that insulin (10 nM) inhibited apoptosis and up-regulated the protein expression levels of pAKT, pGSK3β, β-catenin of HT22 cells induced by H 2 O 2 (200 μ M). However, these changes disappeared when the insulin receptors (IR) in HT22 cells were silenced. Taken together, our findings suggested that the impairment of memory in mice induced by dLAN-BL was mediated by insulin via the IR/IRS1/AKT/GSK3β/β-catenin pathway.

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インスリンはIR/IRS1/AKT/GSK3β/β-cateninシグナル経路を介して夜間の薄暗いブルーライトによって誘発される海馬神経細胞のアポトーシスを改善する

近年、環境汚染の一つである夜間の光害が記憶に与える影響が注目されている。しかし、夜間の光、特に夜間の青色光がどのような分子機構で記憶を損なうのかについては、まだ不明な点が多い。そこで、C57BL6/Jマウス42匹を、夜間無光、夜間薄明かり(dLAN-WL)、夜間薄明かり(dLAN-BL)に28日間暴露した。行動学的データでは、dLAN-BLへの曝露により、新規物体認識試験における認識指数および弁別指数の低下から明らかなように、重度の認識記憶障害が生じることが示唆された。同時に、血漿インスリン濃度の低下も観察された。また、これらの変化と一致して、dLAN-BLは海馬のCA1CA3DG領域のニューロン数を減少させ、BaxmRNA発現レベルを上昇させ、Bcl-2Bcl-xlmRNA発現レベルおよびpIRS1pAKTpGSK3ββカテニンのタンパク質発現レベルを低下させることが確認された。In vitro 実験では、インスリン(10 nM)は H 2 O 2200 μM)で誘導された HT22 細胞のアポトーシスを抑制し、pAKTpGSK3ββ-カテニンのタンパク質発現レベルを上昇させることを発見した。しかし、HT22細胞のインスリン受容体(IR)をサイレンシングすると、これらの変化は消失した。以上のことから、dLAN-BL によるマウスの記憶障害は、インスリンが IR/IRS1/AKT/GSK3β/β-catenin 経路を介し ていることが示唆された。

https://www.sciencedirect.com/science/article/pii/S0147651322013288?via%3Dihub

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