Effects of Moringa oleifera aqueous leaf extract in alloxan induced diabetic mice - PubMed (original) (raw)

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Effects of Moringa oleifera aqueous leaf extract in alloxan induced diabetic mice

Muobarak J Tuorkey. Interv Med Appl Sci. 2016 Sep.

Abstract

Objective: There is a lack of knowledge regarding the underlying mechanisms of the antidiabetic activity of Moringa oleifera. This study investigates the antidiabetic effect of M. oleifera and its impact on the immune tolerance.

Methods: Alloxan-induced diabetes model for mice was used. A dose of 100 mg/kg of Moringa extract was orally administered to diabetic treated mice. Glucose and insulin levels were evaluated to calculate insulin resistance. Total antioxidant capacity (TAC), creatinine, and blood urea nitrogen (BUN) levels were measured. The relative percentage of CD44, CD69, and IFN-γ was investigated by flow cytometry.

Results: In diabetic mice, insulin resistance by homeostasis model assessment of insulin resistance (HOMA-IR) was increased 4.5-fold than in the control group, and HOMA-IR was decreased 1.3-fold in the Moringa treatment group. The level of TAC was declined 1.94-fold in diabetic mice, and increased 1.67-fold in diabetic treated group. In diabetic mice, creatinine and BUN levels were significantly reduced 1.42- and 1.2-fold, respectively, in Moringa treatment mice. The relative percentage of CD44 was not changed in diabetic mice, but the relative percentage of CD69 was found to be increased. INF-γ was decreased 2.4-fold in diabetic mice and elevated in treated groups.

Conclusion: Moringa may ameliorate insulin resistance, increase TAC, and improve immune tolerance.

Keywords: blood urea nitrogen; creatinine; immune tolerance; insulin resistance; total antioxidant capacity.

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Figures

Fig. 1.

Fig. 1.

Fasting glucose (A) and insulin (B) levels in different mice involved in this study. Data were expressed as mean ± SE of 10 mice in each group. *P < 0.05, **P < 0.01, and ***P < 0.001, NS: statistically non-significant

Fig. 2.

Fig. 2.

HOMA-IR analysis in different mice involved in this study. HOMA-IR was calculated from glucose (mg/dL) and insulin (μU/mL) levels using the following formula: HOMA = fasting glucose value (mg/dL) × fasting insulin value (μU/mL)/405. Data were expressed as mean ± SE of 10 mice in each group. *P < 0.05, **P < 0.01, and ***P < 0.001, NS: statistically non-significant

Fig. 3.

Fig. 3.

Total antioxidant capacity in different mice involved in this study. Data were expressed as mean ± SE of 10 mice in each group. *P < 0.05, **P < 0.01, and ***P < 0.001, NS: statistically non-significant

Fig. 4.

Fig. 4.

The level of creatinine (A) and blood urea nitrogen (B) levels in different mice involved in this study. Data were expressed as mean ± SE of 10 mice in each group. *P < 0.05, **P < 0.01, and ***P < 0.001, NS: statistically non-significant

Fig. 5.

Fig. 5.

The Fluorescence Minus One gating boundaries for CD44, IFN-γ, and CD69 molecules

Fig. 6.

Fig. 6.

Representative histograms showing the expression of the CD44 molecules in the peripheral blood of different mice involved in this study (A). A representative histogram showing the relative percentage of CD44 molecules (B). Data were expressed as mean ± SE of five mice in each group. *P < 0.05, **P < 0.01, and ***P < 0.001, NS: statistically non-significant

Fig. 7.

Fig. 7.

Representative histograms showing the expression of the CD69 molecules in the peripheral blood of different mice involved in this study (A). A representative histogram showing the relative percentage of CD69 molecules (B). Data were expressed as mean ± SE of five mice in each group. *P < 0.05, **P < 0.01, and ***P < 0.001, NS: statistically non-significant

Fig. 8.

Fig. 8.

Representative histograms showing the expression of IFN-γ molecules in the peripheral blood of different mice involved in this study (A). A representative histogram showing the relative percentage CD69 molecules (B). Data were expressed as mean ± SE of five mice in each group. *P < 0.05, **P < 0.01, and ***P < 0.001, NS: statistically non-significant

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Grants and funding

Funding source: This study was performed by an institutional self support by the author. Author has no commercial interest or other relationship with manufacturers of pharmaceuticals, laboratory supplies, and/or medical devices or with commercial providers of related medical services.

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