The EHFZJ demonstrated a gastroprotective effect at the 400 mg/kg dose in the classical models of acute gastric injury induced by indomethacin, absolute and acidified ethanol. The EHFZJ administration (orally) demonstrated significant inhibition, suggesting a possible physical barrier mechanism exists. The EHFZJ showed no significant differences in terms of percentage of contraction or the speed of wound closure during the observation times (0, 3, 7, 11 and 14 days). The results obtained in this study provide evidence of a potential gastroprotective activity for the Ziziphus joazeiro Mart. Leaf hydroalcoholic extract.Acute pancreatitis is associated with activation of coagulation and there is a close relationship between coagulation and the severity of this disease. Administration of anticoagulants such as heparin or acenocoumarol has shown to reduce the severity of acute pancreatitis and accelerate the recovery. The aim of the current study was to determine the impact of warfarin administration on the course of ischemia/reperfusion-induced acute pancreatitis. Acute pancreatitis was induced in rats by pancreatic ischemia followed by reperfusion. Vehicle (1 ml/dose) or warfarin (45, 90 or 180 μg/kg/dose in 1 ml of vehicle) were administered intragastrically once a day. The first dose of warfarin was given 24 h after the start of pancreatic reperfusion. The severity of acute pancreatitis was assessed 2, 5, 9 and 14 days after the beginning of pancreatic reperfusion. Treatment with warfarin reduces pancreatic damage and accelerates recovery in histological examination and this effect is accompanied by a faster reduction in serum activity of pancreatic digestive enzymes, lipase and amylase. In addition, warfarin led to an earlier decrease in serum concentration of pro-inflammatory interleukin-1β and plasma level of D-dimer. These effects were associated with an improvement of pancreatic blood flow. We conclude that warfarin exhibits a therapeutic effect in acute pancreatitis evoked by pancreatic ischemia followed by reperfusion.Obesity is a major health concern in modern societies as it is linked to diverse chronic diseases, such as diabetes, cancer, stroke, and skeletomuscular disorders. This study aimed to investigate the lipolytic potency of the metabolic suppressor 3-iodothyronamine (T1AM) and its molecular mechanism in differentiated 3T3-L1 adipocytes. Cells stained with Oil Red O showed a remarkable accumulation of lipid droplets by 20-d post-differentiation and a plateau at 26 - 30 day. Treatment with 100 μM T1AM for 6 h increased the liberation of free fatty acids (FFAs) and glycerol (P less then 0.05) detected in the culture media. However, this stimulatory effect was significantly suppressed by ATGListatin, an inhibitor of adipose triglyceride lipase (ATGL), suggesting that ATGL plays a rate-limiting role in triglyceride (TG) turnover. To understand the lipolytic mechanism, immunoblotting and confocal image analyses of the T1AM-treated and control groups were conducted. The elevated lipolysis was accompanied by increases in the phosphorylation of adenosine monophosphate-activated protein kinase (p-AMPK), nuclear localization of forkhead box O1 (FoxO1), and expression of monoacylglycerol lipase (MGL) protein (P less then 0.05). Finally, the treated cells exhibited downregulated expression of acetyl-CoA carboxylase (ACC) relative to p-ACC and increased protein expression of carnitine palmitoyltransferase 1 (CPT1) (P less then 0.05). Taken together, T1AM showed lipolytic potency via activation of the AMPK/FoxO1/ATGL/MGL axis for decomposing TGs to FFAs and glycerol and of the AMPK/ACC/CPT1 pathway in facilitating the mobilization of FFAs into the mitochondria, highlighting its therapeutic potential for the treatment of obesity.It is known that a high level of uric acid (UA) in plasma, hyperuricemia (HU), is associated with the increased risk of cardiovascular diseases (CVDs). Endothelial damage has been suggested as a potential mechanism involved in HU-induced CVDs, especially in patients with the accumulation of other cardiovascular risk factors. However, the role of UA in the pathogenesis of endothelial dysfunction is still a matter of debate. It is unclear whether UA is a causative risk factor in endothelial dysfunction, an inert marker or an endothelium-protective molecule with respect to its antioxidant properties. Of note, only a few studies have been conducted to investigate the effect of UA on vascular endothelium-dependent relaxation. Therefore, we have studied the acute in vitro effects of high UA concentrations on the endothelial function of arteries isolated from aged rats. Experiments were performed in small mesenteric arteries (SMAs), femoral arteries and thoracic aortas isolated from 68-week-old and 57-week-old male Wistar-Kyoto rats. Vascular reactivity was investigated in isometric conditions using the wire myograph and organ chamber. Selleck Molibresib Acetylcholine (ACh) was used to investigate endothelium-dependent vasorelaxation. Then, UA was added to the myograph or organ chamber at 600 μmol/l (arteries from 68-week-old rats) or 1200 μmol/l (arteries from 57-week-old rats) and incubated for 1 h, and this was followed by determining the ACh concentration-response curve. UA had no significant effect on ACh-induced vasorelaxation and pD2 values in all investigated groups. Likewise, no significant differences in noradrenaline- (SMAs), serotonin- (femoral arteries) and phenylephrine-induced (aortas) vasoconstriction were observed after UA pre-incubation. In conclusion, high concentrations of UA administered acutely failed to affect endothelial function and did not provoke endothelial dysfunction in resistant mesenteric arteries, medium-sized and large arteries from aged rats.The increased risk of atherosclerosis in patients with chronic kidney disease (CKD) is associated with the increased concentration of fatty acids from the omega-6 family. Products of arachidonic acid oxidation, including prostaglandins, thromboxanes, hydroxyleicosa-tetraenoic acids (HETES) and hydroxyoctadecadienoic acids (HODES) are involved in the pathogenesis of cancer and cardiovascular diseases due to increased oxidative stress. The aim of our study was to determine the relations resulting from the duration of CKD treatment. One of our main concerns is, whether and when the cascade of synthesis of inflammatory mediators may be insufficient in patients with CKD during many years of treatment. The study involved 121 patients with CKD and 87 healthy volunteers. Eicosanoid profiles 9(S)-HODE, 13(S)-HODE, 5(S)-HETE, 12(S)-HETE, 15(S)-HETE, 5(S)-oxoETE, 16(RS)-HETE, and 5(S),6(R)-lipoxinA4, 5(S),6(R),15(R)-lipoxinA4 were extracted in plasma. The HPLC separations were performed by means of 1260 liquid chromatography.