Neutrophil gelatinase‐associated lipocalin attenuates injury in the rat cecal ligation and puncture model of sepsis via apoptosis inhibition

Abstract

NGAL can attenuate kidney injury and apoptosis in the rat CLP model of sepsis. And the protective effect of NGAL was probably due to the inhibition of apoptosis and lipid peroxidation, and increased expression of HO-1.

Functions and regulation of lipocalin-2 in gut-origin sepsis: a narrative review

“…Lcn2 has been demonstrated to exert protective effects against H 2 O 2 toxicity in vitro [65, 66]. In addition, the presence or administration of Lcn2 induced hypoferremia of inflammation and upregulation of antioxidant enzymes (e.g., superoxide dismutase, heme oxygenase-1) in vivo, to limit iron-induced oxidative stress during sepsis [67, 68]. In other words, Lcn2 might protect against oxidative stress and aid in mitigating intestinal barrier injury.…”

“…In addition to its major role in maintaining local microbiota homeostasis and moderating systemic overactive immune response, Lcn2 has also been reported to protect the gut as well as the lungs, liver, and kidneys from organ failure in sepsis models [28, 48, 67, 68]. Administration of recombinant Lcn2 in vitro to wounded monolayers of colonic epithelial cells promoted cell migration, and its subcutaneous administration in the rat model attenuated indomethacin-induced gastric injury in a dose-dependent manner [24].…”

“…Administration of recombinant Lcn2 in vitro to wounded monolayers of colonic epithelial cells promoted cell migration, and its subcutaneous administration in the rat model attenuated indomethacin-induced gastric injury in a dose-dependent manner [24]. Impaired/delayed liver regeneration in Lcn2-null mice after partial hepatectomy, Lcn2-inhibited renal apoptosis during peritonitis-induced sepsis, and Lcn2-enhanced reparative tubule formation in vitro have also been documented [31, 68, 79]. It is noteworthy that in spite of the contradiction to its foregoing pro-apoptotic effects on myeloid cells, the jury is still out since the apoptosis-related role of Lcn2 is seldom examined in the context of sepsis.…”

New insights into the role of heme oxygenase-1 in acute kidney injury

“…Novel approaches that protect in sepsis models by reducing the inflammatory response and improving renal function also induce HO-1. For example, in the CLP model, such findings have been reported for neutrophil gelatinase-associated lipocalin [78], pachymic acid [79], and honokiol (components of traditional Chinese medicines) [80]. Similarly, in the LPS model, 3,4,5-trihydroxycinnamic acid, a tea extract, is protective and induces HO-1 [81].…”