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02 December 2017 : Laboratory Research  

Protective Effect of Luteolin Against Renal Ischemia/Reperfusion Injury via Modulation of Pro-Inflammatory Cytokines, Oxidative Stress and Apoptosis for Possible Benefit in Kidney Transplant

Yan Liu1BD, Baoxin Shi2C, Yi Li3ABCDE*, Hui Zhang3FG

DOI: 10.12659/MSM.903253

Med Sci Monit 2017; 23:5720-5727

Abstract

BACKGROUND: The acceptances and long-term outcomes of the renal transplantations are seriously jeopardized by inflammatory responses and damage to tissues. The present study intended to explicate the pharmacological effect of luteolin (LT) in renal ischemia/reperfusion (I/R) injury and the possible mechanism of action of LT.

MATERIAL AND METHODS: The effect of LT on the level of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the homogenates of kidney tissues of male Swiss albino mice was determined after I/R injury. The effect of LT on MDA (malondialdehyde), SOD (superoxide dismutase), CAT (catalase), and glutathione were also identified by enzyme assay. In addition, Western blotting was used to determine the level of Bcl-2, Bax, and caspase-3 in the presence of LT.

RESULTS: The results showed that LT caused significant reduction in the level of TNF-α, IL-1β, and IL-6 compared to the I/R group without LT (p>0.05). To further confirm this, the efficacy of LT on the histopathology of I/R injured renal tissues was studied. It was found that LT restored cellular viability of damaged renal tissue. This observation was further confirmed by TUNEL assay, where it was found that LT caused considerable reduction in the population of apoptotic cells. LT pretreatment significantly increased Bcl-2 expression and reduced the level of Bax expression together with a reduction in the level of caspase-3 expression.

CONCLUSIONS: Luteolin showed its effect by interfering and attenuating a number of pathways, including pathways for inflammation and apoptosis in renal tissues.

Keywords: Ischemia

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750