Caftaric acid attenuates kidney and remote organ damage induced by renal ischemia-reperfusion injury

Oxidative stress and inflammation are indispensable components of ischemia-reperfusion (IR) injury. In this study, we investigated the effects of low and high doses of caftaric acid (CA) on reducing kidney and remote organ damage induced by IR. We divided Wistar rats into four groups: sham, IR, low (40 mg/kg body weight (BW)), and high (80 mg/kg BW) CA groups. IR (1 h ischemia, 24 h reperfusion) was applied to all groups, except the sham one. Following the experimental period, we removed kidney and lung tissues to assess biochemical, histopathological, and immunohistochemical parameters. In the IR group, oxidant parameters (malondialdehyde (MDA), myeloperoxidase (MPO), total oxidant status (TOS), oxidative stress index (OSI)) increased, and antioxidant level parameters (superoxide dismutase (SOD) and total antioxidant status (TAS)) diminished. In addition, Microtubule-associated protein light chain 3 (LC3), cyclooxygenase-2 (COX-2), and Caspase-3 immunopositivity were severe in the IR group. CA treatment improved the LC3, COX-2, and Caspase-3 immunopositivity, lowered the oxidant level, and enhanced the antioxidant capacity. Histopathological findings were consistent with the data. In light of all our results, CA is effective against oxidative stress, Autophagy, Apoptosis, and inflammation in the renal IR experimental model.

Acute kidney injury; Apoptosis; Autophagy; Caftaric acid; Ischemia-reperfusion; Lung; Oxidative stress.