Celastrol Improves Isoproterenol-Induced Heart Failure by Reducing Inflammation, Apoptosis and Oxidative Stress

Background and Objective: Celastrol is a pentacyclic triterpenoid with a long history of therapeutic potential. Unfortunately, their prime mechanism for myocardial infarction was unknown. Therefore, the current study has investigated celastrol's efficiency and its cardioprotective role in isoproterenol-induced heart injury. Materials and Methods: The animals have been separated into 4 groups (n = 6). The test group was pretreated with celastrol on the 7th day at the same time as isoproterenol-induced heart damage on the 6th-7th days. The biochemical parameters were determined in serum and heart tissue homogenates. Results: Celastrol significantly decreased the myocardial infarction markers concentration in serum and increased the antioxidant concentration in isoproterenol-induced heart tissue. In addition to this, celastrol also regulates the membrane-bound as well as lysosome enzymes located in the heart tissue. Furthermore, the elevation of pro-inflammatory cytokines and NF-kB mRNA was lessened by celastrol administration. Celastrol also reduced isoproterenol-induced programmed cell death, by altering the Bcl-2, Bax and caspase-3 levels in cardiac tissue. Conclusion: Current findings suggested that administering celastrol may help to reduce cardiac damage in myocardial infarction by reducing inflammation, apoptosis and oxidative stress.