Protective effect of baicalin against severe burn‑induced remote acute lung injury in rats

Abstract

Baicalin exhibits antibacterial, anti‑viral, anti‑oxidative, antipyretic, analgesic, anti‑inflammatory and anti‑tumor properties. The chemical scavenges oxygen free radicals, protects the cardiovascular system and neurons, protects the liver, and has been used for the prevention and treatment of diabetes‑associated complications. The present study investigated the effect of baicalin on severe burn‑induced remote acute lung injury (ALI). The present study demonstrated that baicalin significantly decreased the lung wet‑to‑dry weight ratio, improved pulmonary histological alterations and reduced the expression of high mobility group protein B1 in the rat model of ALI. In addition, treatment with baicalin decreased tumor necrosis factor‑α, interleukin (IL)‑8, IL‑1β and IL‑18 concentrations in the serum, reduced myeloperoxidase activity and malondialdehyde content, and increased the level of superoxide dismutase in the serum in treated model rats with ALI. As a result, baicalin significantly suppressed nucleotide‑binding oligomerization, NACHT, LRR and PYD domains‑containing protein 3 (NLRP3), caspase‑1, nuclear factor‑κB and matrix metalloproteinase‑9 protein expression in the rat model of ALI. The results of the present study suggested that baicalin may serve a protective role against ALI in rats through the NLRP3 signaling pathway.

MicroRNA‑146a/Toll‑like receptor 4 signaling protects against severe burn‑induced remote acute lung injury in rats via anti‑inflammation

“…Factors including traumatic stress, direct injuries of heating power and hypoperfusion may induce the upregulation of expression levels of pro-inflammatory cytokines (2). In addition, these factors may activate a variety of inflammatory cells, including mononuclear macrophages, neutrophil granulocytes, lymphocytes, platelets and endothelial cells (3,4). Furthermore, adhesion molecules of vascular endothelial cells (VECs) and while blood cells (WBCs) have been reported to be upregulated (3,4).…”

“…In addition, these factors may activate a variety of inflammatory cells, including mononuclear macrophages, neutrophil granulocytes, lymphocytes, platelets and endothelial cells (3,4). Furthermore, adhesion molecules of vascular endothelial cells (VECs) and while blood cells (WBCs) have been reported to be upregulated (3,4). The activated WBCs may then induce a respiratory burst and degranulation as the adhesion intensifies.…”

“…Severe burn-induced remote ALI is characterized by the pathological features of a uncontrolled inflammatory response, and it may broadly damage pulmonary VECs and alveolar epithelial cells (4). Severe-burn induced remote ALI has been reported to exhibit morbidity and mortality rates of 20-40% (4). However, no treatments are currently available within intensive care units (4).…”

“…Severe-burn induced remote ALI has been reported to exhibit morbidity and mortality rates of 20-40% (4). However, no treatments are currently available within intensive care units (4). Uncontrollable inflammatory mediators are closely associated with ALI (4).…”

“…However, no treatments are currently available within intensive care units (4). Uncontrollable inflammatory mediators are closely associated with ALI (4). Macrophages were in patients with ALI to induce inflammation (6).…”