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Studies show GHRH agonists like JI-38 improve cardiac function, reduce remodelling, and enhance anti-apoptotic gene expression after myocardial infarction (MI) (8)
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These findings are consistent with previous studies suggesting that Mel and GSH may prevent structural damage in ovarian histoarchitecture by suppressing oxidative stress.10,11,15-18,21,22 Both Mel and GSH are key endogenous antioxidant molecules that neutralize free radicals and preserve tissue integrity by limiting oxidative stress-induced cellular damage.30,31 It has been previously reported that platinum-based chemotherapeutic agents such as carboplatin increase intracellular ROS production, thereby triggering lipid peroxidation (as indicated by elevated MDA levels), inflammatory responses (increased TNF- and IL-6), cellular damage, and apoptosis.2,7,8 In the current study, the increased immunoreactivity of Caspase-3 and NF-B, along with significantly elevated levels of TNF- and IL-6 in the CARB group, indicate that CARB may have simultaneously activated both apoptotic and inflammatory pathways
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