Inhibition of Receptor Interacting Protein Kinases Attenuates Cardiomyocyte Hypertrophy Induced by Palmitic Acid

Figure 3

There is a crosstalk between ER stress and necroptosis in PA-induced cardiomyocyte hypertrophy. (a) Treating the NCMs with PA (200 μM) and OA (250 μM), the mRNA expressions of GRP78, ATF6, and CHOP were increased in PA group, not OA group, . (b) Pretreating the H9c2 cells with pravastatin (10 μM) and effectively blocking the upregulated mRNA expression of GRP78, ATF6, and CHOP (ER stress markers) induced by PA and thapsigargin (100 nM) (an ER stress agonists) via real-time PCR, . (c) Pretreating the H9c2 cells with pravastatin (10 μM) and also effectively blocking the upregulated mRNA expression of RIPK1/RIPK3 induced by PA and thapsigargin via real-time PCR, . (d) The increased protein level of GRP78 and CRT in NCMs was downregulated by pravastatin (10 μM) (western blot), . Data in (a), (b), (c), and (d) are expressed as mean ± SD, indicates compared to control treatment, and indicates compared to PA treatment.

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