Abstract: To assess the effect of apigenin (API), a functional food factor, on 3-chloro-1,2-propanediol (3-chloro 1, 2-propanediol, 3-MCPD)-induced mitochondrial fission and fusion, the protective effect of API on renal injury was investigated. A total of 36 male adult Sprague-Dawley rats were randomly divided into six groups of 6 animals each: control group, solvent control (sodium carboxymethyl cellulose) group, 3-MCPD group, and low-, middle- and high-dose apigenin group. Rats in the experimental groups were administrated via oral gavage with 3-MCPD (30 mg/kg mb) alone or in combination with apigenin at different doses for 28 days. Body mass and food intake were recorded daily during the experimental period. Finally, the rats were sacrificed to harvest kidney, liver and brain tissues. Rinal tissue sections, stained with hematoxylin and eosin, were observed by microscopy. Renal mitochondrial fission and fusion and transcription factor expression were examined. The results showed that apigenin significantly alleviated the loss of appetite, renal tissue swelling, the increase of kidney/body mass ratio, the irregularity of renal tubular and collecting ducts epithelium and glomerular and renal capsular lesions in rats exposed to 3-MCPD. In addition, apigenin significantly attenuated the up-regulation of DRP1 and FIS1 and the down-regulation of MFN1, MFN2, PGC1, NRF1 and TFAM. At the protein level, apigenin alleviated the increase of mitochondrial fission, the decrease of mitochondrial fusion and the down-regulation of transcription factor NRF2 induced by 3-MCPD. This study suggested that apigenin could protect rats from 3-MCPD induced renal injury via up-regulating the expression of mitochondrial transcription factors and alleviating abnormal mitochondrial fusion and fission.

Key words: apigenin, 3-chloro-1,2-propanediol, renal injury, mitochondrial fission and fusion, mitochondrial transcription factor