Cilostazol Protects Against Sepsis-Induced Kidney Impairment in a Mice Model

Sepsis is a type of systemic inflammatory disease caused by polymicrobial infection. To investigate the potential reno-protective benefits of cilostazol during sepsis-induced renal injury, forty male albino Swiss mice, 25 to 30 grams in weight and 8 to 12 weeks old, were employed in the present investigation. Both food and water were freely available to these animals. Mice were separated into the following four groups after two weeks of adaption. (n = 10): (1) Healthy group: apparently normal mice. (2) induced group: mice underwent cecal ligation and puncture operation. (3) DMSO group: mice received DMSO as a vehicle (4) cilostazol group: Cilostazol was administered intraperitoneally to mice for five days in a row at a dose of 5 mg/kg/day. Compared to the CLP group, the cilostazol group showed a significantly (p 0.05) lower amount of NGAL in the kidneys. Additionally, compared to the CLP group, the cilostazol group showed a substantial (p0.05) decline in the levels of serum of inflammatory cytokines (IL-1β, TNF-α, Interleukin-6). Additionally, compared to the CLP group, the cilostazol group had a significantly (p 0.05) increased renal SOD activity and decreased MDA level. Histologically, all animals in the CLP group displayed a substantial level of kidney tissue damage (p 0.05), whereas the cilostazol group displayed a significantly diminished level of kidney tissue injury. Their capacity to lower serum levels of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) has an anti-inflammatory impact. Additionally, they have an antioxidant impact by raising renal SOD activity and lowering renal MDA levels.