Tephrosia purpurea Linn pers Fabaceae a widely growing

Tephrosia purpurea (Linn.) pers, (Fabaceae), a widely growing herbaceous perennial is reported to exhibit significant anti-hyperglycemic activity in animal models [7], [8], [9] as well as able to delay the development of diabetic complications [10], [11]. Recently, we have reported T. purpurea for its beneficial effects in senile cataract, and the activity was correlated with the presence of rutin and quercetin [12]. Both rutin and its aglycone quercetin have been reported previously to possess aldose reductase inhibition [13], [14]. Thus, it could be hypothesized that the effects of T. purpurea extracts on cataract and diabetes might be due to inhibition of AR and reduction of oxidative stress by rutin. Thus, the objective of the present the study was to evaluate the effects of alcoholic extract and flavonoid fraction of T. purpurea in diabetic cataract model and to determine its mechanism of action.
Materials and methods
Results
Discussion Cataract is considered to be a major cause of visual impairment in diabetic patients. Chronic elevation of blood nociceptin receptor in diabetes plays a critical role in the development and progression of major diabetic complications. Prolonged exposure to elevated glucose causes both acute reversible changes in cellular metabolism, and long-term irreversible changes in stable macromolecules. The injurious effects of hyperglycemia are characteristically observed in tissues, which are not dependent on insulin for glucose entry into the cell (e.g., eye lens, kidneys) and, hence, they are not capable of down-regulating glucose transport along with the increase of extracellular sugar concentrations [25]. Moreover, the role of increased oxidative stress is also widely accepted for the development and progression of diabetes and its complications [26]. Reports indicated that diabetic complications are associated with overproduction of free radicals and accumulation of lipid peroxidation by-products [27]. However, many non-enzymatic antioxidants like glutathione (GSH) and enzymatic antioxidants like superoxide dismutase (SOD) are involved in the protection of free radicals induced oxidative damage. Oxygen free radicals are formed disproportionately in diabetes by glucose oxidation, non-enzymatic glycation of proteins and the subsequent oxidative degradation of glycated proteins [28]. Three important mechanisms have been implicated in the development of diabetic cataract i.e. the polyol pathway [29], oxidative stress [30] and formation of advanced glycosylation end products [31], [32]. Although, there is cross talk between these mechanisms, results in several studies suggested that oxidative stress is a major determinant in diabetic complications [33], [34], [35]. Cataract requires not just a surgical solution, but a chemical and pharmacological complement as well. Since, oxidative stress is a common initiator of many diabetic complications, including cataract, chemical approach to delay the onset or retard the progression of cataract is valuable. Therefore, agents or compounds that exert multiple actions, such as antioxidant, hypoglycemic and aldose reductase (AR) inhibitory activity could be more effective therapeutics. Oxidative stress may be a predominant mechanism in STZ-induced hyperglycemia. Oxidative stress may cause direct modification of the inner lens proteins, such as cross-linking, aggregation, and precipitation [36]. The increased TBARS (MDA levels) along with the decreased GSH and altered activities of antioxidant enzymes like SOD in the present study suggested increased oxidative stress in diabetic conditions. Chronic treatment with AcTp and FFTp decreased lipid peroxidation as well as was found effective in restoring the levels of GSH and antioxidant enzymes like SOD. As T. purpurea has been proven to possess potent anti-oxidant activity [37], [38], [39], it is possible that delay in the development of STZ-induced diabetic complications may be predominantly due to its antioxidant activity.