Protective effect of extract from Rumex aquaticus herba on ethanol-induced gastric damage in rats.

BACKGROUND/AIMS: In this study, we investigated the gastroprotective effect of extract including quercetin-3-O-ß-D-glucuronopyranoside (EIQ) from Rumex aquaticus herba against the ethanol-induced gastric damage in rats. METHODS: The rats were divided into eight groups composed of a non-ethanol group, only EIQ (10 mg/kg) group, groups with absolute ethanol after pretreatment with various doses of EIQ (1, 3 and 10 mg/kg), rebamipide (10 mg/kg), stillen (40 mg/kg) and a control receiving only absolute ethanol. Ethanol-induced gastric lesions, lipid peroxidation, neutrophil infiltration and glutathione level were measured. Superoxide dismutase (SOD) and catalase activity were assessed by an assay kit. Protein expression of SOD, catalase or hemoxygenase-1 (HO-1) was assessed by western blotting analysis. RESULTS AND CONCLUSION: In the absolute ethanol treated group, gastric lesion and malondialdehyde levels were significantly increased with enhanced myeloperoxidase activity. Administration of EIQ 1 h prior to ethanol treatment significantly inhibited the formation of gastric lesions and the elevation of the malondialdehyde levels with myeloperoxidase activity. In addition, pretreatment with EIQ significantly increased the level of glutathione, and elevated the activity and protein expression of radical scavenging enzymes, such as SOD, catalase and HO-1. EIQ may exert anti-inflammatory and anti-oxidative effects against ethanol-induced gastric injury through the reduction of lipid peroxidation, myeloperoxidase activity and free radicals.

MLCK and PKC Involvements via Gi and Rho A Protein in Contraction by the Electrical Field Stimulation in Feline Esophageal Smooth Muscle.

We have shown that myosin light chain kinase (MLCK) was required for the off-contraction in response to the electrical field stimulation (EFS) of feline esophageal smooth muscle. In this study, we investigated whether protein kinase C (PKC) may require the on-contraction in response to EFS using feline esophageal smooth muscle. The contractions were recorded using an isometric force transducer. On-contraction occurred in the presence of N(G)-nitro-L-arginine methyl ester (L-NAME), suggesting that nitric oxide acts as an inhibitory mediator in smooth muscle. The excitatory composition of both contractions was cholinergic dependent which was blocked by tetrodotoxin or atropine. The on-contraction was abolished in Ca(2+)-free buffer but reappeared in normal Ca(2+)-containing buffer indicating that the contraction was Ca(2+) dependent. 4-aminopyridine (4-AP), voltage-dependent K(+) channel blocker, significantly enhanced on-contraction. Aluminum fluoride (a G-protein activator) increased on-contraction. Pertussis toxin (a G(i) inactivator) and C3 exoenzyme (a rhoA inactivator) significantly decreased on-contraction suggesting that Gi or rhoA protein may be related with Ca(2+) and K(+) channel. ML-9, a MLCK inhibitor, significantly inhibited on-contraction, and chelerythrine (PKC inhibitor) affected on the contraction. These results suggest that endogenous cholinergic contractions activated directly by low-frequency EFS may be mediated by Ca(2+), and G proteins, such as Gi and rhoA, which resulted in the activation of MLCK, and PKC to produce the contraction in feline distal esophageal smooth muscle.