Water Extract of Mentha x villosa: Phenolic Fingerprint and Effect on Ischemia-Reperfusion Injury.

Qualitative analysis of the water extract of Mentha x villosa Huds. leaves was performed by liquid chromatography mass spectrometry (LC-MS/MS) and quantitative analysis was made by reverse-phase liquid chromatography coupled with photodiode array detection (LC-DAD). Sixteen phenolic compounds were identified and quantified consisting of 8 phenolic acids/derivatives and 8 flavonoid glycosides (quinic acid, chlorogenic acid, coumaroyl-hexoside, caffeic acid, coumaroylquinic acid, lithospermic acid, rosmarinic acid, salvianolic acid A, luteolin-7-O-glucuronide, luteolin-7-O-glucoside, luteolin-7-O-rutinoside, eriodictyol-7-O-rutinoside, apigenin-7-O-glucuronide, kaempferol-3-O-glucuronide, chrysoeriol-7-O-rutinoside, and hesperetin-7-O-rutinoside). Luteolin-7- O-rutinoside (25.6 ± 0.7 mg/g dry extract) and rosmarinic acid (17.9 ± 0.4 mg/g dry extract) were the most abundant. High antioxidant activity of this phenolic-rich water extract was confirmed in vitro by DPPH and ABTS tests and ex vivo in the ischemia-reperfusion injured rat superior mesenteric artery. Thus, the water extract of M. x villosa leaves seems to be a promising agent in prevention of tissue injury caused by oxidative stress.

Efficacy of quercetin derivatives in prevention of ulcerative colitis in rats.

Reactive oxygen species has been implicated to contribute significantly to tissue injury associated with ulcerative colitis. Thus compounds with antioxidant properties could be potential therapeutic agents in this disease. Flavonoid compounds are known to possess antioxidative and antiinflammatory properties. Two derivatives of the flavonoid quercetin (Q), chloronaphthoquinone quercetin (CNC) and monochloropivaloyl quercetin (MCP), showed improved antioxidant properties and moreover, they efficiently inhibited aldose reductase activity in vitro. The aim of the work was to test the potential efficacy of quercetin and these synthetic derivatives in vivo in prevention of intestinal inflammation during ulcerative colitis in rats. Colitis was induced by intracolonic administration of acetic acid (4% solution). The control group received the same volume of saline. The vehicle dimethyl sulfoxide (DMSO) and the drugs Q, CNC or MCP were administered orally two hours and then one hour before the acetic acid or saline instillation. After 48 hours, the animals were sacrificed and the colon was weighed, measured and scored for visible damage. Acetic acid triggered an intense inflammatory response of the colon, characterised by haemorrhage, ulceration and bowel wall thickening. From the drugs tested, only CNC (2 × 50 mg/kg) effectively depressed inflammatory damage of the colon. The mechanism of this beneficial effect remains to be elucidated.

Protection of the vascular endothelium in experimental situations.

One of the factors proposed as mediators of vascular dysfunction observed in diabetes is the increased generation of reactive oxygen species (ROS). This provides support for the use of antioxidants as early and appropriate pharmacological intervention in the development of late diabetic complications. In streptozotocin (STZ)-induced diabetes in rats we observed endothelial dysfuction manifested by reduced endothelium-dependent response to acetylcholine of the superior mesenteric artery (SMA) and aorta, as well as by increased endothelaemia. Changes in endothelium-dependent relaxation of SMA were induced by injury of the nitric oxide radical (·NO)-signalling pathway since the endothelium-derived hyperpolarising factor (EDHF)-component of relaxation was not impaired by diabetes. The endothelial dysfunction was accompanied by decreased ·NO bioavailabity as a consequence of reduced activity of eNOS rather than its reduced expression. The results obtained using the chemiluminiscence method (CL) argue for increased oxidative stress and increased ROS production. The enzyme NAD(P)H-oxidase problably participates in ROS production in the later phases of diabetes. Oxidative stress was also connected with decreased levels of reduced glutathione (GSH) in the early phase of diabetes. After 10 weeks of diabetes, adaptational mechanisms probably took place because GSH levels were not changed compared to controls. Antioxidant properties of SMe1EC2 found in vitro were partly confirmed in vivo. Administration of SMe1EC2 protected endothelial function. It significantly decreased endothelaemia of diabetic rats and improved endothelium-dependent relaxation of arteries, slightly decreased ROS-production and increased bioavailability of ·NO in the aorta. Further studies with higher doses of SMe1EC2 may clarify the mechanism of its endothelium-protective effect in vivo.