Therapeutic Potential of Curcumin, a Bioactive Compound of Turmeric, in Prevention of Streptozotocin-Induced Diabetes through the Modulation of Oxidative Stress and Inflammation

Abstract

This study evaluates the anti-diabetic potential and underlying mechanisms of curcumin in streptozotocin (STZ)-induced type 2 diabetes mellitus (T2DM) rats. The rats were randomly divided into four groups: normal control, negative control (diabetic group), diabetic group receiving glibenclamide (positive control group), and curcumin plus STZ (treatment group). The anti-diabetic activities of curcumin were examined at a dose of 50 mg/kg body weight through physiological, biochemical, and histopathological analysis. Compared to the normal control group rats, elevated levels of glucose, creatinine, urea, triglycerides (TG), and total cholesterol (TC) and low levels of insulin were found in the negative control rats. Curcumin treatment showed a significant decrease in these parameters and an increase in insulin level as compared to negative control rats. In negative control rats, a reduced level of antioxidant enzymes and an increased level of lipid peroxidation and inflammatory marker levels were noticed. Oral administration of curcumin significantly ameliorated such changes. From histopathological findings, it was noted that diabetic rats showed changes in the kidney tissue architecture, including the infiltration of inflammatory cells, congestion, and fibrosis, while oral administration of curcumin significantly reduced these changes. Expression of IL-6 and TNF-α protein was high in diabetic rats as compared to the curcumin treatment groups. Hence, based on biochemical and histopathological findings, this study delivers a scientific suggestion that curcumin could be a suitable remedy in the management of diabetes mellitus.

Keywords: curcumin; diabetes mellitus; inflammation; oxidative stress.

Figure 1

Chemical structure of curcumin.

Figure 2

Role of curcumin on oral glucose tolerance tests (OGTTs) was evaluated. Mean ± SEM was used to describe the findings: * p < 0.05 (significant variance in OGTTs between negative control (NC) and normal control (C)); # p < 0.05 (significant difference between NC and curcumin treatment (CuT)).

Figure 3

The levels of (a) glucose and (b) insulin were measured in different experimental groups of rats (a total of 8 rats in each group). Mean ± SEM was used to define the findings: * p < 0.05 (significant variance in b.w. (final) between negative control (NC) and normal control (C)); ** p < 0.05 (significant difference between NC and curcumin treatment (CuT)).

Figure 4

The serum levels of triglycerides (TG) and total cholesterol (TC) were evaluated in rats (8 rats in each group). Mean ± SEM was used to define the findings: * p < 0.05 (significant variance in b.w. (final) between negative control (NC) and normal control (C)); ** p < 0.05 (significant difference between NC and curcumin treatment (CuT)).

Figure 5

The serum levels of creatinine and total urea were evaluated in rats (a total of 8 rats in each group). Mean ± SEM was used to define the findings: * p < 0.05 (significant variance in b.w. (final) between negative control (NC) and normal control (C)); ** p < 0.05 (significant difference between NC and curcumin treatment (CuT)).

Figure 6

The MDA levels were evaluated in rats (a total of 8 rats in each group). Mean ± SEM was used to define the findings: * p < 0.05 (significant variance in b.w. (final) between negative control (NC) and normal control (C)); ** p < 0.05 (significant difference between NC and curcumin treatment (CuT)).

Figure 7

The measurement of antioxidant enzyme levels in rats (a total of 8 rats in each group). Mean ± SEM was used to define the findings: * p < 0.05 (significant variance in b.w. (final) between negative control (NC) and normal control (C)); ** p < 0.05 (significant difference between NC and curcumin treatment (CuT)).

Figure 8

Cytokine levels were measured in rats (a total of 8 rats in each group). Mean ± SEM was used to define the findings: * p < 0.05 (significant variance in b.w. (final) between negative control (NC) and normal control (C)); ** p < 0.05 (significant difference between NC and curcumin treatment (CuT)).

Figure 9

Renal tissue architecture of different experimental groups of rats: (a) normal control group; (b) STZ-induced negative control group rats; (c) STZ treated with curcumin (50 mg/kg body weight); (d) STZ treated with glibenclamide (positive control). Original magnification: 100×; scale bar: 50 μm. The red arrow shows inflammatory cells and the blue arrow shows congestion.

Figure 10

Renal tissue fibrosis in different experimental groups of rats: (a) normal control group; (b) STZ-induced diabetic group; (c) STZ treated with curcumin (50 mg/kg body weight; (d) STZ treated with glibenclamide. Original magnification: 100×; scale bar: 50 μm. Arrow (yellow) showing collagen fiber deposition.

Figure 11

Renal tissue fibrosis in different experimental groups of rats: (a) normal control group; (b) STZ-induced negative control group; (c) STZ treated with curcumin (50 mg/kg body weight); (d) STZ treated with glibenclamide (positive control). Original magnification: 100×; scale bar: 50 μm. Arrow (green) showing fiber deposition.

Figure 12

(A) Expression of IL-6 protein in different experimental groups of rats: (a) normal control group (showed no expression); (b) STZ-induced negative control group (showed high expression); (c) STZ treated with curcumin (50 mg/kg body weight) (showed less expression); (d) STZ treated with glibenclamide (positive control, showed no expression). Original magnification: 100×; scale bar: 50 μm. Arrow (red) showing cytoplasmic positivity. (B) Graph showing IL-6 expression in different experimental groups: * p < 0.05 (significant variance in b.w. between negative control (NC) and normal control (C)); ** p < 0.05 (significant difference between NC and curcumin treatment (CuT)).

Figure 13

(A) Expression of TNF-α protein in different experimental groups of rats: (a) normal control group (showed no expression); (b) STZ-induced negative control group (showed high expression); (c) STZ treated with curcumin showed decreased expression; (d) STZ treated with glibenclamide (positive control, showed no expression). Original magnification: 100×; scale bar: 50 μm. Arrow (red) showing cytoplasmic positivity. (B) Graph showing TNF-α expression in different experimental groups: * p < 0.05 (significant variance in b.w. between negative control (NC) and normal control (C)); ** p < 0.05 (significant difference between NC and curcumin treatment (CuT)).