Abstract
This study tested the protective effect of maslinic acid (MA) against diabetic retinopathy (DR) in rats with type 1 diabetes mellitus (T1DM) and investigated possible mechanisms of action. DM was introduced by streptozotocin (STZ) (65 mg/kg, i.p.). Control and STZ (T1DM) were divided into 2 subgroups, which received either the vehicle or MA (80 mg/kg). Serum, pancreases, and retinas were collected for further use. MA significantly reduced fasting glucose levels in the control and T1DM rats but enhanced fasting insulin levels and partially increased the size of the islets of Langerhans and the number of β-cells in T1DM rats. In addition, MA significantly improved the retina structure by preventing the reduction in the area between the inner and outer limiting membranes (ILM and OLM, respectively) and increasing the number of cells forming the ganglion cell layer (GCL), inner nuclear layer (INL), and outer nuclear layer (ONL). Associated with these effects, MA significantly reduced the total levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), as well as the nuclear levels of NF-κB p65, mRNA levels of Bax, and protein levels of cleaved caspase-3 in the retinas of T1DM rats. However, MA significantly lowered levels of reactive oxygen species (ROS) and malondialdehyde (MDA) but significantly increased the nuclear levels of Nrf2, protein levels of Bcl2, and total levels of superoxide dismutase (SOD) and reduced glutathione (GSH) in the retinas of the control and T1DM rats. In conclusion, MA prevents DR by antioxidant potential mediated by the activation of Nrf2.
Highlights
Diabetes mellitus (DM) is a chronic world pandemic disorder and is the 4th leading cause of death worldwide due to the development of several microvascular and microvascular complications [1]
DM can be either type 1 DM (T1DM) that is characterized by complete loss of insulin or T2DM that is associated with insulin resistance (IR) and peripheral insulin ineffectiveness [1]
Diabetic retinopathy (DR) is a major cause of visual impairment and blindness among diabetic patients [4, 5]. e disease can be classified into two major types according to the time of the development, an early nonproliferative DR (NPDR), and a more advanced later type, the proliferative one (PDR)
Summary
Diabetes mellitus (DM) is a chronic world pandemic disorder and is the 4th leading cause of death worldwide due to the development of several microvascular and microvascular complications [1]. The DR is a vascular oxidant and inflammatory disorder in which locally produced reactive oxygen species (ROS) and inflammatory cytokines and chemokines mediate their pathogenesis and are the major triggers for all other well-known damaging events [10–14] Both hyperglycaemia and systemic inflammation play significant roles in this process but seem to be dependent on the type of diabetes. Both hyperglycaemia and systemic inflammation are major triggers of DR in T2DM patients, whereas systemic inflammation has a limited role in T2DMinduced DR [15] Within this view, increased influx of the systemic inflammatory cytokines is an independent factor that can initiate the damage in the diabetic retina by damaging the BRB, increasing the vascular permeability, exaggerating ROS generation, activating microglial cells and macrophage infiltration, and enhancing pericytes and neural apoptosis [10, 16, 17]. Erefore, in the study, we have evaluated the ability of MA to prevent diabetic retinopathy in STZ-induced T1DM in rats and investigated some of its mechanisms of action
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