Preclinical evidence 4
4 studies reported at therapy level; 4 evidence entries itemised.
MouseChemical/toxin
Model: Acute pancreatitis with associated intestinal epithelial disruption
BML-111 increased E-cadherin, reduced apoptosis and reactive oxygen species and lessened pancreatic and intestinal injury, and these protective effects were abolished in Nrf2 deficient cells and Nrf2 knockout mice.
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RatOtherSprague-DawleyMale
Model: Fat embolism syndrome-induced acute lung injury
Fat embolism increased lung injury score, wet-to-dry ratio, BALF protein, leukocytes, neutrophils, myeloperoxidase, TNF-alpha and IL-1beta, alongside raised lipoxin A4 and upregulated ALX/FPR2. BML-111 lowered the inflammatory response, and this benefit was attenuated by the ALX/FPR2 antagonist BOC…
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RatEndotoxin/LPSSprague-Dawley
Model: Lipopolysaccharide-induced acute lung injury and lipopolysaccharide plus D-galactosamine induced acute liver injury
BML-111 protected against lipopolysaccharide-induced acute lung injury and lipopolysaccharide plus D-galactosamine induced acute liver injury, repressing angiotensin converting enzyme activity and increasing ACE2 activity, with all effects reversed by the lipoxin receptor inhibitor BOC-2.
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MouseEndotoxin/LPSBALB/cn = 128 mice randomly allocated to four groupsPretreatment before induction of pancreatitis
Model: Acute pancreatitis-associated lung injury produced by seven hourly intraperitoneal injections of cerulein followed immediately by a single dose of Escherichia coli lipopolysaccharide (two-hit model)
Pretreatment with BML-111 lowered serum amylase, TNF-alpha and IL-1 beta, raised IL-10, reduced lung wet to dry weight ratio and pancreatic and pulmonary histological injury scores, and increased pulmonary heme oxygenase-1 expression compared with the untreated injury group.
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