Protective effects of Ulinastatin on oxidative stress and inflammation of rat-derived cardiomyocytes H9c2.

Ischemic heart disease (IHD) is a common clinical disease and has a younger tendency in recent years. This study focused on the role of Ulinastatin (UTI) in the anti-oxidative stress and anti-inflammatory response of cardiomyocytes. H9c2 cells were divided into control group, ischemia-anoxic group (ischemic hypoxia group) and ischemia-anoxia + UTI group (UTI group). Cell morphology was observed by light microscopy, Cell staining, Western blotting, quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were conducted to research the effect of UTI on the nuclear factor-κB (NF-κB) signaling pathway. H9c2 cells in the ischemic hypoxia group showed hypertrophy and irregular shape, while the cell morphology of the UTI group was close to the fusiform shape. The cell hypertrophy was lighter, and the number of irregular morphological cells decreased in UTI group than ischemic hypoxia group. The content of interleukin-1β (IL-1β) in the ischemic hypoxic group was significantly higher than that in the control group. In the UTI group, IL-1β was significantly lowly expressed than the ischemia hypoxia group. In addition, the expressions of SOD1, SOD2, GPX1, GPX3, Bcl-2 and Sirt1 in UTI group were higher than ischemic hypoxia group (P<0.05). The expressions of p65, Iκk-α kinase, Caspase3 and Bax in UTI group were lower than ischemic hypoxia group (P<0.05). UTI protects H9c2 cells from ischemia and hypoxia injuries by inhibiting the NF-κB pathway, thereby reducing inflammation, resisting oxidative stress, inhibiting apoptosis, and delaying cell senescence.