上海
Hemin chloride（氯化血红素），化学本质为铁原卟啉IX氯化物（Fe³⁺-protoporphyrin IX chloride），是血红素的铁 (III) 类似物，也是一种血红素加氧酶 (HO)-1 诱导剂。具有两种生物学效应：既能激活内源性保护通路，也能在特定条件下诱发氧化损伤。
Hemin chloride（CAS No.：16009-13-5）首先能通过诱导血红素氧合酶-1（HO-1）表达发挥抗氧化与抗炎作用，在小鼠肺纤维化、结肠炎及心肌梗死模型中显著降低MDA、TNF-α、IL-6等氧化与炎症标志物，并调控AMPK/SIRT1/PGC-1α/HO-1/NF-κB及TGF-β1/MAPK信号通路[1]；Hemin chloride还能调控KEAP1/NRF2通路（抑制KEAP1介导的NRF2泛素化，促进其核转位并上调GCLC、xCT等基因）以维持细胞稳态[2]。在诱导氧化损失方面，Hemin chloride还能催化产生活性氧（ROS），触发铁依赖性脂质过氧化、铁死亡或坏死性凋亡，研究表明Hemin chloride在寡突胶质细胞中以3.3–10 μM浓度即能选择性损伤髓鞘与轴突，此外Hemin chloride在HT-22神经元中还能通过RIP1/RIP3通路介导细胞死亡[3]。还有文献证实Hemin chloride能作为ANO1通道抑制剂（IC50 = 0.45 μM）诱导前列腺癌细胞凋亡。在血液系统研究中，Hemin chlorideHemin chloride（AbMole，M9092）能用于诱导红细胞分化，探究血红蛋白合成机制及动物血液系统疾病的发病机理。Hemin chloride动物实验中，腹腔注射常用剂量为5–10 mg/kg。Hemin chloride在结肠炎模型中5–10 mg/kg/day连续给药14天显著改善病理指标且未见肝肾毒性；在小鼠肾缺血再灌注模型中5 mg/kg呈现时间依赖性双重效应（激活内源性保护通路与诱导氧化损伤） [4]。
参考文献及鸣谢
[1] Hao, W.; Yu, T. T.; Li, W.; et al. Hemin attenuates bleomycin-induced lung fibrosis in mice by regulating the TGF-beta1/MAPK and AMPK/SIRT1/PGC-1alpha/HO-1/NF-kappaB pathways. The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 2024, 28 (6), 559-568.
[2] Georgiou-Siafis, S. K.; Tsiftsoglou, A. S. Activation of KEAP1/NRF2 stress signaling involved in the molecular basis of hemin-induced cytotoxicity in human pro-erythroid K562 cells. Biochemical pharmacology 2020, 175, 113900.
[3] Su, X.; Wang, H.; Lin, Y.; et al. RIP1 and RIP3 mediate hemin-induced cell death in HT22 hippocampal neuronal cells. Neuropsychiatric disease and treatment 2018, 14, 3111-3119.
[4] Estarreja, J.; Caldeira, G.; Silva, I.; et al. The Pharmacological Effect of Hemin in Inflammatory-Related Diseases: A Systematic Review. Biomedicines 2024, 12 (4).
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