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莱菔硫烷 3α-O-β-D-吡喃葡萄糖苷介导的低血糖及其对链脲佐菌素诱导的糖尿病小鼠损伤肾脏中凋亡调控蛋白表达的影响。

Lyoniresinol 3α-O-β-D-glucopyranoside-mediated hypoglycaemia and its influence on apoptosis-regulatory protein expression in the injured kidneys of streptozotocin-induced mice.

机构信息

Pharmaceutical College, Guangxi Medical University, Nanning, Guangxi, China.

出版信息

PLoS One. 2013 Dec 3;8(12):e81772. doi: 10.1371/journal.pone.0081772. eCollection 2013.

DOI:10.1371/journal.pone.0081772
PMID:24312585
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3849267/
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.

摘要

杨桃(酢浆草科)根(ACLR)在传统中药中用于治疗糖尿病和糖尿病肾病(DN)已有悠久的历史。(±)-Lyoniresinol 3α-O-β-D-吡喃葡萄糖苷(LGP1、LGP2)是从 ACLR 中分离出的两种手性木质素葡萄糖苷。本研究旨在探讨 LGP1 和 LGP2 介导的降血糖作用对链脲佐菌素(STZ)诱导的糖尿病小鼠肾脏损伤的影响。STZ 诱导的糖尿病小鼠连续 14 天口服给予 LGP1 和 LGP2(20、40、80mg/kg 体重/天)。LGP1 处理可显著降低高血糖和核因子-κB(NF-κB)、半胱氨酸天冬氨酸蛋白酶-3、-8、-9 和 Bcl-相关 X 蛋白(Bax)等相关蛋白的表达。然而,LGP2 处理没有降血糖活性。LGP1 治疗可改善糖尿病依赖的肾脏改变,如肾小球肥大、细胞外基质过度积聚、肾小球和肾小管基底膜增厚。B 细胞淋巴瘤白血病-2(Bcl-2)在 STZ 诱导的糖尿病小鼠肾脏中的表达减少,但 LGP1 处理可增强其表达。这些发现表明,LGP1 治疗可能抑制糖尿病肾病的进展,并可能调节治疗或预防糖尿病肾病的几个药理学靶点。

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