Salidroside ameliorates sepsis-induced acute lung injury and mortality via downregulating NF-κB and HMGB1 pathways through the upregulation of SIRT1.

Sepsis is a life-threatening medical condition. Salidroside, a substance isolated from Rhodiola rosea, possesses antioxidant and anti-inflammatory properties. The effect and mechanism of salidroside on sepsis-induced acute lung injury still remains to be well clarified.

C/EBP homologous protein deficiency aggravates acute pancreatitis and associated lung injury.

Aim: To investigate the pathophysiological role of C/EBP homologous protein (CHOP) in severe acute pancreatitis and associated lung injury.

Methods: A severe acute pancreatitis model was induced with 6 injections of cerulein (Cn, 50 μg/kg) at 1-h intervals, then intraperitoneal injection of lipopolysaccharide (LPS, 7.5 mg/kg) in CHOP-deficient (Chop(-/-)) mice and wild-type (WT) mice.

Honokiol attenuates the severity of acute pancreatitis and associated lung injury via acceleration of acinar cell apoptosis.

Severe acute pancreatitis remains a life-threatening disease with a high mortality rate among a defined proportion of those affected. Apoptosis has been hypothesized to be a beneficial form of cell death in acute pancreatitis. Honokiol, a low-molecular-weight natural product, possesses the ability of anti-inflammation and apoptosis induction.

Honokiol rescues sepsis-associated acute lung injury and lethality via the inhibition of oxidative stress and inflammation.

Purpose: Sepsis has a high mortality rate despite the recent advances in intensive care medicine and antibiotics. Honokiol, a low molecular weight natural product, is known to possess anti-inflammatory activity. Here, we investigate whether honokiol can ameliorate acute lung injury and lethal response in murine models of sepsis.

Uropathogenic Escherichia coli-induced inflammation alters mouse urinary bladder contraction via an interleukin-6-activated inducible nitric oxide synthase-related pathway.

Escherichia coli is the most common cause of urinary tract infection. Elevated blood and urine interleukin-6 (IL-6) levels have been shown in inflammatory urinary tract diseases. The role of IL-6 in mediating the urodynamic dysfunction in response to E.

Inhibition of NADPH oxidase-related oxidative stress-triggered signaling by honokiol suppresses high glucose-induced human endothelial cell apoptosis.

Angiopathy is a major complication of diabetes. Abnormally high blood glucose is a crucial risk factor for endothelial cell damage. Nuclear factor-kappaB (NF-kappaB) has been demonstrated as a mediated signaling in hyperglycemia or oxidative stress-triggered apoptosis of endothelial cells.

Uropathogenic Escherichia coli alters muscle contractions in rat urinary bladder via a nitric oxide synthase-related signaling pathway.

Background: Uropathogenic Escherichia coli (UPEC) is a common cause of urinary-tract infection. The mechanisms by which bacteria cause the symptoms of cystitis remain unclear.

Methods: The contractions of isolated rat detrusor strips evoked by electrical field stimulations (EFS) or by exogenous agonists and immunoblotting for the detection of protein expression in the bladder were measured in the short (1 h) and long (24 h) term after the intravesical instillation of J96 (O4:K6) strain or UPEC isolated from patients with acute E.