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It helps to reverse neuronal apoptosis caused by ischemic stroke and promotes the repair of damaged tissue (Liu et al., 2023), showing great potential in research into ischemic stroke, Alzheimers disease, and other disorders

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Its probable mechanism includes activation of renal AGE-RAGE signaling pathways, decreasing levels of monocyte chemotactic protein-1 (MCP-1) and PKC-A, which consequently reduces the production of slit diaphragm proteins such as nephrin and podocin, thereby mitigating the impact of AGE-mediated DN pathogenesis (Muthenna et al., 2014)