| Description | Hemin is an iron-containing porphyrin. Hemin is an Heme oxygenase (HO)-1 inducer. |
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| Related Catalog | Signaling Pathways >> Autophagy >> Autophagy Signaling Pathways >> Autophagy >> Mitophagy Research Areas >> Cardiovascular Disease |
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| Target | Heme oxygenase[1] |
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| In Vitro | Hemin and PGJ2, used as positive controls, strongly increase both expression and activity of HMOX after 4 and 12 h, respectively. Indeed, a significant effect is found of 30 μM Hemin on cell proliferation in all used cell lines after 48 h, which is dose-dependent. Hemin treatment decreases cell proliferation to 62±5 %, 51±3 %, and 38±8 % in PA-TU-8902, BxPC-3 and MiaPaCa-2 cancer cells, respectively, with p<0.0001 for all comparisons. Furthermore, enhancement of anti-proliferative effects of statins is observed by Hemin, documented as decreased cell proliferation after 48 h of co-treatment[1]. |
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| In Vivo | Following the i.p. administration of Hemin (100 μmol/kg), the HO-1 level in the renal cortex begins to increase gradually. The HO-1 level reaches its peak 24 h after Hemin preconditioning. HO-1 is expressed mainly in the renal tubules. The HO-2 level in the kidney does not change following Hemin preconditioning[2]. |
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| Cell Assay | For the cell proliferation assay, cells are seeded into 96 well (5-12.5×104 cells per mL according to the cell line) and kept at 37°C and 5 % CO2. After 24 h, cells are treated with statins or/and Hemin, followed by the MTT test as a general cell proliferation assay[1]. |
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| Animal Admin | Mice[2] Eight- to ten-week-old male BABL/c mice are used for the ischemia-reperfusion (I/R) experiments. The animals are divided into five groups as follows: (1) the sham group undergo isolation of the bilateral renal arteries without clamping; (2) the vehicle group receive an intraperitoneal (i.p.) injection of 4 mL/kg PBS as a vehicle control (with IRI); (3) the Hemin-preconditioned group receive Hemin, a potent inducer of HO-1, at 100 μmol/kg i.p.; (4) the Hemin plus ZnPP group receive zinc protoporphyrin IX, an inhibitor of HO-1 activity, at 5 mg/kg i.p. 6 h after receiving 100 μmol/kg Hemin i.p.; and (5) the Hemin plus PD98059 group receive PD98059, an inhibitor of ERK1/2 activity, at 10 mg/kg i.p. 6 h after receiving 100 μmol/kg Hemin i.p. Both inhibitors are administered i.p. 2 h before I/R, whereas Hemin was administered 8 h before I/R. |
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| References | [1]. Vanova K, et al. Heme oxygenase is not involved in the anti-proliferative effects of statins on pancreatic cancer cells. BMC Cancer. 2016 May 12;16:309. [2]. Chen HH, et al. Heme oxygenase-1 ameliorates kidney ischemia-reperfusion injury in mice through extracellular signal-regulated kinase 1/2-enhanced tubular epithelium proliferation. Biochim Biophys Acta. 2015 Oct;1852(10 Pt A):2195-201. |
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