Troxerutin is a semi-synthetic bioflavonoid rutin derivative that has recently fascinated a lot of study attention due to its pharmacological properties [1, 2]. TRX, vitamin P4; 3,4,7-Tris[O-(2- hydroxyethyl)] rutin is found in tea, coffee, cereals, fruits and vegetables. Because of its high water solubility, it readily absorbed in GIT with less toxicity on tissues [3, 4]. It has been indicated that TRX have several pharmacological effects including antioxidative, antiinflammatory, antihyperlipidemic, and nephroprotective, improving learning and memory impairments induced by A? [1, 5, 6]. Many studies have been shown that TRX has antineoplastic, antithrombotic and antifibrinotic effects [6].
Some reports have indicated TRX has protective role in many tissues such as brain, kidney, heart, vascular damages and liver [3]. It is also inhibited testicular toxicity induced by nickel in rats [6]. Moreover, troxerutin has beneficial activity in insulin resistance and diabetes as well as improves testicular function and sperm production in prepubertal type 1 diabetic male rats via reducing oxidative stress [7]. Oxidative stress is an imbalance between free radicals such as ROS and RNS and antioxidant systems.
Free radicals with an uneven electron can lead to large chain chemical reactions with important macromolecules like proteins, nucleic acids and membrane fatty acids. Therefore, oxidative stress can disrupt the function of these macromolecules and lead to apoptosis [8]. Oxidative stress is involved in many pathological conditions such as cancer, Parkinson disease, Alzheimer diseases, heart failure, diabetes and depression [9]. A study on wistar rats has indicated that TRX has protective effect on hippocampal neurons against oxidative stress and apoptosis induced by amyloid-beta, due to decrease in MDA level and increase in SOD and GPX activity [1]. Similarly, TRX improves oxidative stress in blood of streptozotocin-induced type-1 diabetic rats via decreasing in MDA level; the major product of lipid peroxidation, elevating in the activity of antioxidant enzymes SOD, GPX, and CAT compared with diabetic groups with no significant effect on non-diabetic rats [10]. An investigation on mice fed calorie-rich diet, has illustrated that TRX prevents mitochondrial oxidative stress and myocardial apoptosis, due to decrease in ROS production, lipid peroxidation, proapoptotic proteins (APAF-1, BAX, caspases-9 and-3 and increase in antiapoptotic protein (BCL-2)[11]. A research shows that troxerutin prevents BDE-47-induced kidney cell apoptosis through antioxidation and antiapoptosis activity [3]. Two main regulators of oxidative stress and inflammation are Nrf2 and NF-?B [12, 13]. TRX shows anticancer properties in hepatocarcinoma cell line via increasing nuclear translocation of Nrf2, decreasing oxidative stress and suppressing the expression of IKK?, therefore downregulates NF-?B mediated inflammation and proliferation [14]. Similarly, due to reduce in ROS levels, NF ?B protein expression and Akt activation, TRX protects against diabetic cardiomyopathy in a rat model of type 2 diabetes [15].
The purpose of this paper is to review the recent scientific reports regarding TRX, its antioxidative effect and potential role as therapeutic agent, to provide a photo of the chemistry, and to elucidate the effects that TRX might have on patients.