| Abstrakt: |
Systemic chronic inflammation may cause kidney injury as a result of an impaired immune response and pro-inflammatory cytokine overload due to various factors that prevent the resolution of inflammation. Therefore, it is important to determine pro-inflammatory cytokine levels by renal biopsy and to investigate treatment modalities in systemic chronic inflammation-related kidney injury. We aimed to investigate the therapeutic effect of methylprednisolone on extra-renal systemic chronic inflammation-induced renal tissue damage in terms of histopathological alterations and immunohistochemically on tumor necrosis factor-α, interleukin-1β, and interleukin-6 levels. The mice used in this study were divided into three equally sized groups (n: 10). Group I (control) received 0.3 mL 0.9% NaCl, and group II received 0.3 mL complete Freund's adjuvant-casein emulsion intraperitoneally for systemic chronic inflammation induction. Group III received methylprednisolone 10 mg/kg intramuscularly after intraperitoneal injection of 0.3 mL complete Freund's adjuvant-casein emulsion. Injections were administered on days 1 and 14 of the study, and the experiment was ended 5 week after the second injections following the development of systemic chronic inflammation. Finally, kidney tissues were examined histopathologically and immunohistochemically for tumor necrosis factor-α, interleukin-1β, and interleukin-6 levels. While normal renal histology was observed in group I, glomerulonephritis and tubulointerstitial nephritis findings were detected in group II and group III. Methylprednisolone treatment decreased the histopathologic lesions observed in group III. Immunostaining with anti-tumor necrosis factor-α, interleukin-1β and interleukin-6 showed severe immunopositivity in group II and mild immunopositivity in group III, whereas they were immunonegative in group I. Our study provides histopathological and immunohistochemical evidence supporting the decreasing effect of methylprednisolone on tumor necrosis factor-α, interleukin-1β, and interleukin-6 levels in kidney tissue against SCI-induced renal damage due to excessive pro-inflammatory cytokine overload. [ABSTRACT FROM AUTHOR] |
