Mechanism of antidiabetic effects of Plicosepalus Acaciae flower in streptozotocin-induced type 2 diabetic rats, as complementary and alternative therapy

Abstract

Background: Diabetes and its related complications remain to be a major clinical problem. We aim to investigate the antidiabetic mechanistic actions of Plicosepalus Acaciae (PA) flowers in streptozotocin (STZ)-induced diabetic rats.

Methods: After diabetes induction, rats were divided randomly into five groups, including: 1) normal control group, 2) diabetic control group, 3) diabetic group treated with 150 mg/kg of ethanolic extract of PA flowers, 4) diabetic group treated with 300 mg/kg of ethanolic extract of PA flowers, and 5) diabetic group treated with 150 mg/kg of metformin. After 15 days of treatment; fasting blood glucose, glycated hemoglobin (HBA1c%), insulin, C-peptide, superoxide dismutase (SOD), catalase, reduced glutathione (GSH), malondialdehyde (MDA), triglyceride (TGs), total cholesterol (Tc), low density lipoprotein cholesterol (LDL-c), very LDL (VLDL), high DLc (HDL-c), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were assessed. Histopathology of pancreas was also assessed.

Results: The results showed that PA flower ethanolic extract significantly reduced blood glucose, HBA1c%, MDA, TGs, Tc, VLDL, LDL-c, TNF-α, and IL-6 levels in a dose-dependent manner. All these parameters were already increased by diabetic induction in the untreated diabetic group. Treatment of diabetic rats with PA flower increased insulin, HDL-c, GSH, catalase, and SOD levels. Histological examination showed that the PA flower caused reconstruction, repair, and recovery of damaged pancreas when compared with the untreated group.

Conclusions: PA flower has a potential role in the management of diabetes as complementary and alternative therapy, due to its antioxidant, anti-inflammatory, hypolipidemic, hypoglycemic and insulin secretagogue effects.

Keywords: Antioxidant; Diabetes; Metformin; Plicosepalus Acaciae; Quercetin; Streptozotocin.

Fig. 1

Histological effects of normal saline [b, c, & d], PA flower ethanolic extract (150 mg/kg) [e, f, & g], PA flower ethanolic extract (300 mg/kg) [h, i, & j] and Metformin (150 mg/kg) [k, l, & m] treatments on pancreatic sections in streptozotocin induced diabetic rats in comparison with non-diabetic healthy pancreatic section [a]. These figures were showed a normal architecture of pancreatic acini & normal islet of Langerhans in non-diabetic control [a], while a reduction in β-cell number i.e., destruction of the islet of Langerhans (*) [b] with a necrosis in a pancreatic acini (arrows) [c], fatty changes in pancreatic acini (interstitial vaculation ➔ arrow) [d] in pancreas of normal saline treated diabetic rats. Moreover, there was a reduction in the size of pancreatic islets; atrophied islets of Langerhans (arrows) [e], with a slight hemorrhage in the islets of beta cells (red color) [f & g] in pancreas of PA (150 mg/kg) treated diabetic rats. A reduction in the size of islets; atrophied islet of Langerhans (arrow) [h], with a slight hemorrhage in the pancreatic acini (arrow) [i], and a recovering from necrosis in the pancreatic acini [j] of PA (300 mg/kg) treated diabetic rats, while a hemorrhage in a pancreatic acini congestion (red color) [k], with a reduction in number of beta cells, hemorrhage [l], and slight minimal necrotic cells (arrows) [m] in the pancreatic acini of Metformin (150 mg/kg) treated diabetic rats (H & E 400X; Scale bar = 50 μm)

Fig. 2

The diagrammatic illustration of PA mechanisms as alternative and complementary therapy for diabetes mellitus. (−) = Inhibition, (+) = Activation, ↑ = Increase, ↓ = Decrease, CRP = C-reactive protein, TNF-α = tumor necrosis factor-alpha, IL-6 = interlukin-6, SGPT = serum glutamate pyruvate transaminase, SGOT = serum glutamate oxaloacetate transaminase, ALR2 = aldose reductase 2, FFA = free fatty acid, TGs = triglycerides, Oxd. LDL-c = oxidized low-density lipoprotein cholesterol, NADPH = reduced nicotinamide adenine dinucleotide phosphate, GSH = reduced glutathione, SOD = superoxide dismutase, MAPK = mitogen activated protein kinase, IR-β = insulin receptor β, ERK1/2 = extracellular signal regulated kinase1/2