RESUMEN
Asthma is an inflammatory disease of the airways of the lungs, which is characterized by airflow obstruction and bronchospasms. Glabridin is a major flavonoid, especially found in root of Glycyrrhiza glabra, and has several pharmacological activities, including antioxidant and anti-inflammatory effects. The anti-asthmatic effect and possible mechanism of glabridin, however, have not been revealed so far. The aim of this study is to investigate the effects and possible mechanisms of glabridin against ovalbumin (OVA)-induced airway hyperresponsiveness (AHR) and inflammation in mice. In male BALB/c mice, asthma was induced by intraperitoneal (i.p) injection of OVA mixed with 2 mg aluminium hydroxide on days 0, 14 and boosted with OVA aerosol challenge on days 21, 22, and 23. Mice were either treated with dexamethasone (i.p, 1 mg/kg) or glabridin (10, 20, and 30 mg/kg) from days 18-23. Pulmonary function parameters such as peak inspiratory flow, peak expiratory flow, tidal volume, expiratory volume, the frequency of breathing, enhanced pause values were evaluated by using whole-body plethysmography. Measurements were performed at baseline and following methacholine (50 mg/mL) challenges. In addition, white blood cells (WBC) count, total protein, and IgE levels were measured in bronchial alveolar lavage fluid (BALF), lung, and serum, respectively. Glabridin (20 or 30 mg/kg) significantly attenuated (p < 0.05) OVA-induced alteration in respiratory parameters. Elevated counts of total WBC, differential WBC (neutrophils, lymphocytes, monocytes, and eosinophils) in BALF and the total protein in lungs and BALF were significantly decreased (p < 0.05) by glabridin (20 or 30 mg/kg). It also significantly attenuated the increased serum IgE levels (p < 0.05). As glabridin reduces the level of serum IgE, the total protein and the count of WBC and improves respiratory function, it may be a novel therapeutic agent in asthma.
Asunto(s)
Asma , Hiperreactividad Bronquial , Animales , Líquido del Lavado Bronquioalveolar , Modelos Animales de Enfermedad , Inflamación , Isoflavonas , Pulmón , Masculino , Ratones , Ratones Endogámicos BALB C , Ovalbúmina , FenolesRESUMEN
Inflammation, and the pain that accompanies it, is a natural response of the body. The licorice plant (Glycyrrhiza glabra) have demonstrated anti-inflammatory, anti-edematous, and anti-nociceptive effects of its extracts. The effective ingredient remains unidentified; however, one possibility is the unique isoflavone glabridin. The anti-nociceptive, and anti-inflammatory effects of glabridin and its possible mechanism with focus on the large conductance Ca2+-activated K+ (BKCa) channels and L-arginine-nitric oxide (NO) pathway were examined by using different tests. In order to determine the anti-edematous, anti-nociceptive, and anti-oxidative effects of glabradin, some tests such as the tail flick, hotplate, carrageenan-induced paw edema, air pouch, acetic-acid-induced writhing, formalin, and capsaicin tests, as well as toxicity and open field tests were made. Glabridin was administered to rats (n = 8) or mice (n = 8) for 3 d at 3 doses (10, 20, and 40 mg/kg). Glabridin inhibited cytokine production and showed an anti-nociceptive response via the activating of BKCa channels and downregulating NO level and partially transient receptor potential vanilloid-1 pathways. It also demonstrated anti-inflammatory effects by inhibiting cyclooxygenase (COX) activity, while showing no cytotoxicity. Glabridin, however, showed no anti-nociceptive effect in the neurogenic phase. Glabridin is a promising substance in terms of its anti-nociceptive and anti-inflammatory effects by disrupting peripheral NO production, inhibiting cyclic guanosine monophosphate (cGMP) activation and activating BKCa channels and its lack of acute and subacute toxic effects.
Asunto(s)
Analgésicos/uso terapéutico , Antiinflamatorios/uso terapéutico , Edema/tratamiento farmacológico , Isoflavonas/uso terapéutico , Canales de Potasio de Gran Conductancia Activados por el Calcio/metabolismo , Dolor/tratamiento farmacológico , Fenoles/uso terapéutico , Analgésicos/farmacología , Analgésicos/toxicidad , Animales , Antiinflamatorios/farmacología , Antiinflamatorios/toxicidad , Citocinas/inmunología , Edema/inmunología , Edema/metabolismo , Isoflavonas/farmacología , Isoflavonas/toxicidad , Dosificación Letal Mediana , Leucocitos/efectos de los fármacos , Leucocitos/fisiología , Masculino , Ratones Endogámicos BALB C , Óxido Nítrico/metabolismo , Dolor/inmunología , Dolor/metabolismo , Fenoles/farmacología , Fenoles/toxicidad , Ratas WistarRESUMEN
BACKGROUND: Propofol is an intravenous anesthetic that can be used for the induction and maintenance of anesthesia. In the present study, it was aimed to investigate the mechanism of vasodilator action of propofol in the rat aorta (RA). METHODS: The RA rings were suspended in isolated organ baths and tension was recorded isometrically. First, potassium chloride (KCl) and phenylephrine (PE) were added to organ baths to form precontraction. When the precontractions were stable, propofol (1, 10, and 100 µM) was added cumulatively to the baths. The antagonistic effect of propofol on KCl (45 mM), PE (1 µM), 5-hydroxytryptamine (5-HT) (30 µM), and calcium chloride (CaCl2) (10 µM to 10 mM) induced contractions in the vascular rings were investigated. Propofol-induced relaxations were also tested in the presence of the K+ channel inhibitors tetraethylammonium (TEA, 1 mM), glibenclamide (GLI, 10 µM), 4-aminopyridine (4-AP, 1 mM), and barium chloride (BaCl2, 30 µM). RESULTS: Preincubation with propofol (1, 10, and 100 µM) did not affect the basal tone but inhibited the contraction induced by KCl, PE, 5-HT, and CaCl2-induced contractions. Propofol-induced relaxation was not effected by 4-AP, GLI, and BaCl2. However, TEA inhibited propofol-induced relaxations significantly. CONCLUSIONS: The propofol induces relaxation in contracted RA and inhibits KCl, PE, 5-HT, and CaCl2-induced contractions. The results demonstrate that the mechanism of action of propofol-induced vasodilation in the RA may be related to large conductance Ca2+-activated K+ channel activation.
Asunto(s)
Aorta/efectos de los fármacos , Subunidades alfa de los Canales de Potasio de Gran Conductancia Activados por Calcio/agonistas , Propofol/farmacología , Vasodilatación/efectos de los fármacos , Vasodilatadores/farmacología , Animales , Aorta/metabolismo , Femenino , Técnicas In Vitro , Subunidades alfa de los Canales de Potasio de Gran Conductancia Activados por Calcio/metabolismo , Ratas Wistar , Transducción de SeñalRESUMEN
Aim and Introduction: Rosa damascena is one of the most well-known species of the Rosaceae family and is widely used in the food and perfume industry. Rose hydrosol is a product which is produced by distillation of rose petals. There is very little research about the antimicrobial effect of rose hydrosol. In this study, we aimed to investigate the antibacterial effect of Rosa damascena hydrosol in vivo. Method: 45 adult volunteers who were not healthcare workers were included in this study. Exclusion criteria included existing skin disorders or lacerations, pregnancy, presence of nail polish, recent handwashing or use of antiseptic lotion/soap in the last week, and antibiotic use in the last 3 months. At baseline, each subject was asked to rub the fingertips of the dominant hand on a sheep-blood agar plate. The subjects were randomly divided into two groups: one group rubbed their hands with 3 mL of alcohol-based hand antiseptic and the other group with 3 mL of rose hydrosol. Following sample collection, the subjects were asked to rub their hands according to the World Health Organization's (WHO) "How to Hand Rub" technique. After the hand-rubbing sequence, the hands were allowed to air-dry and fingertip sampling was performed. Culture plates were evaluated by a microbiologist blinded to group assignment. Rose hydrosol was analysed by gas chromatography/mass spectrometry. Results: The main components of rose hydrosol are phenyl ethyl alcohol, beta-citronellol and geraniol. Of the total of 45 participants, 23 were included in rose hydrosol group and 22 in the alcohol-based hand-rub group. The colony counts decreased significantly in the alcohol-based solution group after hand-rubbing, whereas there was no significant reduction in the rose hydrosol group. Conclusion: A number of studies have shown good antimicrobial activity in rose products, especially in rose oil, but we found no antibacterial effect of rose hydrosol after hand-rubbing. However, it must be borne in mind that the amount and types of rose hydrosol components are highly influenced by the given agro-meteorological conditions and technological production methods.
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The present study aimed to investigate the role of cannabinoid 2 (CB2) receptors in a rat model of acute inflammation. Therefore, the potential of anti-inflammatory effects of CB2 receptor agonist (GW405833), CB2 receptor antagonist (AM630), and diclofenac, were investigated in carrageenan induced paw oedema in rats: as were assessed by measuring paw oedema; myeloperoxidase (MPO) activity in paw tissue; malondialdehyde (MDA) concentration; glutathione (GSH) level in paw tissue for oxidant/antioxidant balance; cytokine (interleukin-1ß, IL-1ß; tumour necrosis factor-α, TNF-α) levels in serum; histopathology of paw tissue for inflammatory cell accumulations. The results showed that GW405833 or diclofenac significantly reduced carrageenan-induced paw oedema. GW405833 also inhibited the increase of MPO activity, the recruitment of total leukocytes and neutrophils, and MDA concentration during carrageenan-induced acute inflammation, along with reversed nearly to the normal levels the increased of TNF-α, and IL-1ß in serum. AM630 did not affect inflammation alone however clearly reversed the effects of agonist when co-administered. The mechanism of GW405833's suppression of inflammation is supported by these results, which are achieved by the inhibition of neutrophil migration, which regulates the reduction of oxidative stress, TNF-α and IL-1ß levels. Finally, the activation of CB2 receptor, by selective agonist, has a major role in peripheral inflammation, and in the near future, targeting the peripheral cannabinoid system as a promising alternative to treat inflammation diseases may be considered a novel pharmacologic approach.
RESUMEN
Despite the development of modern medicine, alternative medicine, which has not lost its timeliness, remains attractive for the treatment of various diseases. Glabridin, a major flavonoid of Glycyrrhiza glabra, is known for its antioxidant and anti-inflammatory activity. The aim of this study was: 1) to determine the possible protective role of glabridin against ischemia/reperfusion (I/R) injury of the intestine; 2) to evaluate the in vitrocontractile responses of ileum smooth muscles to acetylcholine after an intestinal I/R; and 3) to explain the underlying molecular mechanism of its effect. Rats were assigned to groups of six rats each; 1) I/R, 2) gla10, 3) gla20, 4) gla40, 5) N5-[imino(nitroamino)methyl]-L-ornithine, methyl ester monohydrochloride (L-NAME)+gla40, and 6) Sham group. The healing effect of glabridin was abolished by L-NAME. Glabridin did not cause contractility of the smooth muscles to acetylcholine-induced contractile responses in intestinal I/R. Yet, it increased to spontaneous basal activity.
A pesar del desarrollo de la medicina moderna, la medicina alternativa, sin perder su vigencia, sigue siendo atractiva para el tratamiento de varias enfermedades. Glabradina, el flavonoide mayoritario de Glycyrrhiza glabra, es conocido por su actividad antioxidante y antiinflamatoria. Los propósitos de este estudio fueron: 1) Determinar el posible rol protector de glabradina ante daños intestinales por isquemia/reperfusion (I/R) 2) Evaluar in vitrolas respuestas de contracción de los músculos lisos del ileum ante acetilcolina después de I/R intestinal; y 3) Explicar el mecanismo molecular subyacente de este efecto. Se asignaron grupos de seis ratas: 1) I/R, 2) gla10, 3) gla20, 4) gla40, 5) N5-[imino(nitroamino)metil]-L-ornithina, metil ester monohidrochloruro (L-NAME)+gla40, y 6) Grupo testigo. El efecto curativo de glabridina fue abolido por L-NAME. Glabridina no causó contracción en el músculo liso como respuesta acetilcolina-inducida I/R. Además, incrementa la actividad basal expontánea.