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Tropical Journal of Pharmaceutical Research

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Curcumin ameliorates renal impairment in a diabetic rat model

Peiling Bao, Xiaoyan Wu, Sai Xie, Tao Li, Aiqiao Feng

Abstract


Purpose: To investigate the molecular mechanisms of action of curcumin in regulating kidney injury in diabetic rats.

Methods: Diabetes was induced in male Wistar rats by intraperitoneal administration of streptozotocin (STZ). The rats were divided into four groups, labelled as follows: blank control, positive control of curcumin-untreated STZ-rats, curcumin-treated STZ-rats (20 mg/kg), and curcumin-treated STZ-rats (50 mg/kg). After 24 weeks, blood glucose, HbA1c, mean arterial pressure (MAP), heart rates, and body weights were measured. Fasting blood samples were also collected for albumin, lipocalin-2, osteopontin, and kidney-injury-molecule 1 (KIM1) The samples were also evaluated by enzyme linked immunosorbent assay (ELISA). Rat kidneys were isolated for assessment of renal impairment by haematoxylin and eosin staining (H&E), TUNEL assays, polymerase chain reaction (PCR), and western blotting.

Results: Compared with STZ group, STZ + Cur (50 mg/kg) group significantly decreased blood glucose (284.57 ± 4.28 mg/dL, p < 0.01 vs. STZ), HbA1c (5.22 ± 0.33 %, p < 0.01 vs. STZ), and MAP (76 ± 2 mmHg, p < 0.05 vs. STZ), heart rate (300 ± 6 bpm, p < 0.05 vs. STZ), and body weight (356 ± 6 g, p < 0.01 vs. STZ) were significantly increased. Kidney protein index was significantly increased, indicating improvement of renal pathological damage. The inflammatory and apoptotic cells were less than that of the STZ group in the renal tissues. The mRNA abundance and relative protein expression levels of Wnt 5a and β-catenin were also enhanced. Curcumin regulation of the Wnt signal pathway was inhibited by protease inhibitor, XAV-939.

Conclusion: These results demonstrated that curcumin treatment in diabetic rats alleviates renal damage by regulating Wnt signal pathway.

Keywords: Curcumin, Renal impairment, Diabetes, Wnt signal pathway




http://dx.doi.org/10.4314/tjpr.v18i2.8
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