タキシフォリンとアスティルビンは,Nrf2/HO-1シグナル伝達により,鶏の肝細胞におけるカドミウム誘発の酸化ストレスとアポトーシスから保護する
Tiezhu Chen1,2, Tianyu Han3,4, Yusong Miao5
1Sichuan Academy of Chinese Medicine Sciences, Chengdu, 610042, China.
Biological trace element research
|August 29, 2025
まとめ
アスティルビン (ASB) とタクシーフォリン (TAX) は,Nrf2抗酸化経路を活性化することによって,カドミウム毒性から鶏肝臓を保護します. これらの天然化合物は酸化ストレスとアポトーシスを軽減し,重金属汚染物質から家禽の健康を守ります.
科学分野:
- 環境毒理学
- 動物科学
- 生物化学
背景:
- カドミウム (Cd) は食物連鎖に蓄積する広範囲にわたる重金属汚染物質です.
- 鶏はCdの毒性に対して敏感で,肝臓が主な標的器官である.
- Cdによる肝損傷のメカニズムと潜在的な緩和戦略を理解することは,動物の健康と食品の安全性にとって極めて重要です.
研究 の 目的:
- カドミウム被曝が鶏の肝臓損傷を引き起こすメカニズムを調査する.
- カドミウムによる肝損傷に対するアスティルビン (ASB) とタクシーフォリン (TAX) の保護効果の評価.
- カドミウム毒性におけるNrf2抗酸化経路の役割とASBとTAXによる緩和を調査する.
主な方法:
- コントロール,ASB,TAX,Cd + ASB,Cd + TAX,Cdグループに分割されたハイライン茶色の雄鶏によるin vivo試験.
- カドミウムとメタロチオネインのレベル,肝臓組織の組織学 (H&E) と超構造的 (TEM) 検査.
- 酸化ストレスマーカー,Nrf2抗酸化システムの活性化,および肝臓組織におけるアポトーシス関連因子の調査.
主要な成果:
- カドミウム曝露は肝臓損傷,酸化ストレス増加,鶏のアポトーシスマーカーの変化をもたらした.
- アスティルビン (ASB) とタクシーフォリン (TAX) は,Nrf2/HO-1信号経路を有意に活性化し,Nrf2核転移を促進しました.
- ASBとTAX治療は抗酸化酵素活性 (GSH,SOD,T-AOC) を増加させ,Cd誘発のアポトーシスを軽減し,肝臓組織を保護した.
結論:
- アスティルビンとタクシーフォリンは,家禽におけるカドミウムによる肝損傷に対する有意な保護効果を示しています.
- 保護メカニズムには,Nrf2/HO-1抗酸化経路の活性化とアポトーシスの調節が含まれます.
- これらの発見は,食用動物における重金属の毒性を軽減する天然剤としてのASBとTAXの可能性を強調しています.
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