Bacha Mohsinul Mulk, Nadeem Humaira, Zaib Sumera, Sarwar Sadia, Imran Aqeel, Rahman Shafiq Ur, Ali Hafiz Saqib, Arif Muazzam, Iqbal Jamshed
Department of Pharmaceutical Chemistry, RIPHAH Institute of Pharmaceutical Sciences G-7/4, Islamabad, Pakistan.
Department of Biochemistry, Faculty of Life Sciences, University of Central Punjab, Lahore, 54590, Pakistan.
BMC Chem. 2021 Apr 27;15(1):28. doi: 10.1186/s13065-021-00756-z.
In diabetes, increased accumulation of sorbitol has been associated with diabetic complications through polyol pathway. Aldose reductase (AR) is one of the key factors involved in reduction of glucose to sorbitol, thereby its inhibition is important for the management of diabetic complications. In the present study, a series of seven 4-oxo-2-thioxo-1,3-thiazolidin-3-yl acetamide derivatives 3(a-g) were synthesized by the reaction of 5-(4-hydroxy-3-methoxybenzylidene)-4-oxo-2-thioxo-1,3-thiazolidin-3-yl acetic acid (2a) and 5-(4-methoxybenzylidene)-4-oxo-2-thioxo-1,3-thiazolidin-3-yl acetic acid (2b) with different amines. The synthesized compounds 3(a-g) were investigated for their in vitro aldehyde reductase (ALR1) and aldose reductase (ALR2) enzyme inhibitory potential. Compound 3c, 3d, 3e, and 3f showed ALR1 inhibition at lower micromolar concentration whereas all the compounds were more active than the standard inhibitor valproic acid. Most of the compounds were active against ALR2 but compound 3a and 3f showed higher inhibition than the standard drug sulindac. Overall, the most potent compound against aldose reductase was 3f with an inhibitory concentration of 0.12 ± 0.01 µM. In vitro results showed that vanillin derivatives exhibited better activity against both aldehyde reductase and aldose reductase. The molecular docking studies were carried out to investigate the binding affinities of synthesized derivatives with both ALR1 and ALR2. The binding site analysis of potent compounds revealed similar interactions as were found by cognate ligands within the active sites of enzymes.
在糖尿病中,山梨醇的积累增加通过多元醇途径与糖尿病并发症相关。醛糖还原酶(AR)是参与将葡萄糖还原为山梨醇的关键因素之一,因此抑制醛糖还原酶对于糖尿病并发症的治疗很重要。在本研究中,通过5-(4-羟基-3-甲氧基亚苄基)-4-氧代-2-硫代-1,3-噻唑烷-3-基乙酸(2a)和5-(4-甲氧基亚苄基)-4-氧代-2-硫代-1,3-噻唑烷-3-基乙酸(2b)与不同胺的反应,合成了一系列七种4-氧代-2-硫代-1,3-噻唑烷-3-基乙酰胺衍生物3(a - g)。对合成的化合物3(a - g)进行了体外醛还原酶(ALR1)和醛糖还原酶(ALR2)的酶抑制潜力研究。化合物3c、3d、3e和3f在较低的微摩尔浓度下表现出对ALR1的抑制作用,而所有化合物都比标准抑制剂丙戊酸更具活性。大多数化合物对ALR2有活性,但化合物3a和3f表现出比标准药物舒林酸更高的抑制作用。总体而言,对醛糖还原酶最有效的化合物是3f,其抑制浓度为0.12±0.01μM。体外结果表明,香草醛衍生物对醛还原酶和醛糖还原酶均表现出更好的活性。进行了分子对接研究,以研究合成衍生物与ALR1和ALR2的结合亲和力。有效化合物的结合位点分析揭示了与酶活性位点内同源配体相似的相互作用。