Vyas Neera, Mehra Rakhi, Makhija Renu
Assistant Director (Med.), Central Council for Research in Ayurvedic Sciences, Janakpuri, New Delhi, India.
Department of Clinical research, Central Ayurveda Research Institute for Cardio Vascular Diseases, Punjabi Bagh, New Delhi, India.
Ayu. 2016 Apr-Jun;37(2):92-97. doi: 10.4103/ayu.AYU_134_13.
species plant has been used traditionally as an Ayurvedic medicine for diabetes mellitus. Studies over the past decades have shown its multi-targeted role in diabetics. In the present review article, various mechanisms of action of on diabetics are discussed in detail. Apart from the well-known action of decreasing postprandial glucose sugar by inhibiting α-glucosidase and α-pancreatic amylase, it also inhibits aldose reductase which otherwise results in microvascular complications. Importantly, its peroxisome proliferator-activated receptor (PPAR)-γ agonist (such as thiazolidinediones, the insulin sensitizers) action increases the uptake of free fatty acid (FFA) and facilitates their storage in subcutaneous fat rather than the visceral fat. This reduces plasma FFA and insulin resistance. Furthermore, it increases the expression of and translocation to the cell surface of glucose transporter 1 and 4 receptors which result in glucose uptake by the liver and skeletal muscle and decreases plasma glucose levels. It also decreases inflammatory cytokines and increases adiponectin expression. as PPAR-α agonist (such as fibrates) has a role in the management of dyslipidemia. The activation of PPAR-α leads to the increased expression of lipoprotein lipase and apolipoprotein (Apo) A-V and decrease in hepatic Apo-C-III. These actions lower plasma triglycerides in chylomicrons and very low-density lipoprotein particles, thus liberating fatty acids, which are taken up and stored as fat in adipocytes. has been shown to suppress the overexpression of cardiac PPAR-α (similar to angiotensin-converting enzyme inhibitors/angiotensin receptor blockers) and thereby preventing diabetic cardiomyopathy. It also suppresses the cardiac angiotensin II Type 1 receptors resulting in antihypertrophic and antifibrogenic effect.
该植物物种传统上被用作治疗糖尿病的阿育吠陀药物。过去几十年的研究表明其在糖尿病患者中具有多靶点作用。在本综述文章中,详细讨论了该植物对糖尿病患者的各种作用机制。除了通过抑制α-葡萄糖苷酶和α-胰淀粉酶降低餐后血糖这一众所周知的作用外,它还抑制醛糖还原酶,否则该酶会导致微血管并发症。重要的是,其过氧化物酶体增殖物激活受体(PPAR)-γ激动剂(如噻唑烷二酮类,胰岛素增敏剂)作用可增加游离脂肪酸(FFA)的摄取,并促进其在皮下脂肪而非内脏脂肪中的储存。这降低了血浆FFA和胰岛素抵抗。此外,它增加葡萄糖转运蛋白1和4受体的表达并使其转位至细胞表面,从而导致肝脏和骨骼肌摄取葡萄糖并降低血浆葡萄糖水平。它还可减少炎性细胞因子并增加脂联素表达。该植物作为PPAR-α激动剂(如贝特类药物)在血脂异常管理中发挥作用。PPAR-α的激活导致脂蛋白脂肪酶和载脂蛋白(Apo)A-V的表达增加,以及肝脏Apo-C-III的减少。这些作用降低了乳糜微粒和极低密度脂蛋白颗粒中的血浆甘油三酯,从而释放脂肪酸,这些脂肪酸被脂肪细胞摄取并储存为脂肪。该植物已被证明可抑制心脏PPAR-α的过度表达(类似于血管紧张素转换酶抑制剂/血管紧张素受体阻滞剂),从而预防糖尿病性心肌病。它还抑制心脏血管紧张素II 1型受体,产生抗肥厚和抗纤维化作用。