Key result
Ticagrelor protected renal function in a mouse model of sepsis-induced acute kidney injury by inhibiting platelet activity, inflammation, neutrophil recruitment, and cell apoptosis.
Why the study?
Does ticagrelor protect renal function in a mouse model of sepsis-induced acute kidney injury?
Does ticagrelor protect renal function in a mouse model of sepsis-induced acute kidney injury?
In a mouse model of sepsis-induced acute kidney injury, ticagrelor protected renal function by inhibiting inflammation, neutrophil recruitment, and apoptosis.
Ticagrelor merits testing in human sepsis-AKI trials; leaves open whether benefits translate beyond this mouse model.
Platelets are traditionally considered to be essential components of primary hemostasis. Recent investigations have revealed that platelets can be activated in patients with sepsis and are implicated in the development of sepsis and sepsis-induced-acute kidney injury (SAKI). In the present study, ticagrelor was used to induce a mouse model of SAKI by cecal ligation and puncture. It was found that ticagrelor could inhibit platelet activity, decrease the levels of interleukin-1β and serum creatinine, reduce infiltration of neutrophils in renal tissue, and attenuate cell apoptosis in the kidney. The results suggested that ticagrelor could protect renal function by inhibiting inflammation, recruitment of neutrophils into the kidney, and cell apoptosis in renal tissue. Thus, the findings might provide new strategies for preventing SAKI.
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Li et al. (2018) studied Sepsis-induced acute kidney injury (SAKI). Ticagrelor was evaluated on Renal function, inflammation, neutrophil infiltration, and cell apoptosis. Ticagrelor protected renal function in a mouse model of sepsis-induced acute kidney injury by inhibiting platelet activity, inflammation, neutrophil recruitment, and cell apoptosis.
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