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Fig. 8. Schematic illustration of the protective mechanism of curcumin against renal ischemia/reperfusion injury (IRI). The mechanism involves suppression on activation of c-Jun N-terminal kinase (JNK) pathway via epigenetic regulation of p300/CREB-binding protein (CBP)-mediated histone acetylation. In the IRI rat model, JNK activation promotes the elevation in acH3K9 level at caspase-3/-9 gene promoters, as well as the occupancy of p300/CBP on the gene promoters. These events can enhance caspase-3/-9 expression, thereby resulting in renal cell apoptosis involved in IRI. Curcumin can attenuate these changes through its effects on JNK signaling and histone acetylation.
Korean J Physiol Pharmacol 2021;25:413-423
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