The Effects of Iloprost on Isthmin-1, Adropin and Trpc6 Immunoreactivity in an Experimental Lower Extremity Ischemia–Reperfusion Injury Model
İbrahim Murat Özgüler, Latif Üstünel, Tuncay KuloğluBackground and Objectives: Ischemia–reperfusion (IR) injury to skeletal muscle induces both structural and functional impairments, primarily attributed to increased production of reactive oxygen species and subsequent inflammation following reperfusion. Iloprost (ILO), a stable prostacyclin analog, exerts cytoprotective effects through reduction in oxidative stress as well as by improvement of microvascular function. The purpose of the present study was to investigate the influence of iloprost on Isthmin-1 (ISM-1), adropin and transient receptor potential canonical 6 (TRPC6) immunoreactivity in rat lower extremity muscles in an experimental IR model. Materials and Methods: Thirty male Wistar albino rats, were divided into five groups, each with an equal number of rats; Control, Sham, ILO, IR, and IR + ILO. The ILO group received an intravenous infusion of 2 ng/kg/min ILO. After intracardiac blood was collected, muscle tissue samples were rapidly removed. Serum total oxidant status (TOS) and total antioxidant status (TAS) levels were measured. Histopathological examination of the collected muscle tissue samples was performed using hematoxylin-eosin staining, and immunohistochemical staining was used to assess the immunoreactivity of ISM-1, adropin, and TRPC6. Results: The IR group showed increased serum total oxidant status levels and immunoreactivity for ISM-1, adropin, and TRPC6, while total antioxidant status levels decreased. Compared with the IR group, the IR + ILO group showed decreased serum TOS levels and immunoreactivity for ISM-1, adropin, and TRPC6, while TAS levels increased. Conclusions: Treatment with ILO may have a protective effect on the skeletal muscle of lower extremities exposed to ischemia–reperfusion injury. This effect may be due to a reduction in oxidative stress and the regulation of immunoreactivity of ISM-1, adropin, and TRPC6.