Hemin (Hemin chloride) is a chlorinated iron-containing porphyrin, a heme oxygenase (HO)-1 inducer. Hemin has therapeutic activity in porphyrias by reducing heme deficiency in patients, thereby inhibiting δ-aminolevulinic acid synthetase activity through biochemical feedback.

METHODS: Pancreatic cancer cells PA-TU-8902, BxPC-3 and MiaPaCa-2 were treated with Hemin (30 µM) for 48 h. Cell viability was measured using the CellTiter-Glo Luminescent Cell Viability Assay.
RESULTS: Hemin had a significant effect on cell proliferation of PA-TU-8902, BxPC-3 and MiaPaCa-2 cell lines, decreasing cell proliferation to 62±5%, 51±3% and 38±8%, respectively. [1]
METHODS: Astrocyte cultures were treated with Hemin (25 µM) for 12-24 h. Iron content was measured using colorimetric method.
RESULTS: Iron accumulation occurred in cultured astrocytes after incubation with Hemin. [2]

METHODS: To investigate the effects on renal injury, Hemin (100 µmol/kg) was administered intraperitoneally to BABL/c mice with renal ischemia-reperfusion.
RESULTS: Hemin pretreatment promoted ERK1/2 phosphorylation and enhanced tubular recovery, thereby preventing further kidney injury. [3]
METHODS: To investigate the effects on insulin resistance, Hemin (50 µmol/kg) was administered intraperitoneally to C57BL/6 mice on a high-fat diet once daily for four weeks.
RESULTS: Hemin prevented the development of high-fat diet-induced insulin resistance by increasing insulin sensitivity in skeletal muscle. [4]

In vitro effects of various statins and hemin, a heme oxygenase inducer, on cell proliferation were evaluated in PA-TU-8902, MiaPaCa-2 and BxPC-3 human pancreatic cancer cell lines. The effect of statins on heme oxygenase activity was assessed and heme oxygenase-silenced cells were used for pancreatic cancer cell proliferation studies. Cell death rate and reactive oxygen species production were measured in PA-TU-8902 cells, followed by evaluation of the effect of cerivastatin on GFP-K-Ras trafficking and expression of markers of invasiveness, osteopontin (SPP1) and SOX2[1].