Abstract
Averrhoa carambola L. (Oxalidaceae) root (ACLR) has a long history of use in traditional Chinese medicine for treating diabetes and diabetic nephropathy (DN). (±)-Lyoniresinol 3α-O-β-D-glucopyranoside (LGP1, LGP2) were two chiral lignan glucosides that were isolated from the ACLR. The purpose of this study was to investigate the effect of LGP1 and LGP2-mediated hypoglycaemia on renal injury in streptozotocin (STZ)-induced diabetic mice. STZ-induced diabetic mice were administrated LGP1 and LGP2 orally (20, 40, 80 mg/kg body weight/d) for 14 days. Hyperglycaemia and the expression of related proteins such as nuclear factor-κB (NF-κB), caspase-3, -8, -9, and Bcl-associated X protein (Bax) were markedly decreased by LGP1 treatment. However, LGP2 treatment had no hypoglycaemic activity. Diabetes-dependent alterations in the kidney such as glomerular hypertrophy, excessive extracellular matrix amassing, and glomerular and tubular basement membrane thickening were improved after 14 days of LGP1 treatment. B cell lymphoma Leukaemia-2 (Bcl-2) expression was reduced in the STZ-induced diabetic mouse kidneys but was enhanced by LGP1 treatment. These findings suggest that LGP1 treatment may inhibit diabetic nephropathy progression and may regulate several pharmacological targets for treating or preventing diabetic nephropathy.
Highlights
Diabetes mellitus (DM) is a metabolic disease that is characterized by chronic hyperglycaemia, which is caused by islet β-cell dysfunction and peripheral tissue insulin resistance (IR)
2.6: Fasting blood glucose (FBG) assay During the experiment, fasting blood glucose was measured from the tail vein on d0, d7, and d14 according to the Roche ACCU-CHEK® Performa operation instructions, and the following formula to calculate the FBG descent rate (%)
Increasing amounts of literature have demonstrated that βcell apoptosis is the direct cause of type 1 diabetes, Figure 4. (a) LGP1 treatment alleviated pathological injuries in mouse kidney (HE staining, scale bar: 200 μm). (A) Normal control; (B) Model control; (C) 10mg.kg-1.d-1 of Pioglitazone; (D) 20mg.kg-1.d-1 of LGP1; (E) 40mg.kg-1.d-1 of LGP1; (F) 80mg.kg-1.d-1 of LGP1
Summary
Diabetes mellitus (DM) is a metabolic disease that is characterized by chronic hyperglycaemia, which is caused by islet β-cell dysfunction and peripheral tissue insulin resistance (IR). The active NF-κB triggers the transcription of target genes TNF-α, IL-1β, IL-6, NOS, MCP-1, VCAM-1, ICAM-1, ECAM-1 to increase their gene expression to promote inflammation[9,10] These proinflammatory mediators act as new stimuli to further activate NF-κB and induce the corresponding gene transcription, which results in more low-grade inflammation and a vicious circle. Bcl-2 and Bax family members are apoptosisregulating proteins that play a key role in apoptosis caused by various stimuli. The BuOH extract was successively purified by open repeated silica gel, Sephadex LH-20, ODS column and P-HPLC to obtain LGP1 and LGP2 These compounds were administrated to STZ-induced mice for 14 days with pioglitazone (Pio.) as a positive control to evaluate its hypoglycaemic effect and its anti-apoptotic mechanism, which was relevant to caspase-3, 8, 9, NF-κB, Bcl-2 and Bax
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