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WHO monographs on selected medicinal plants - travolekar.ru

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<str<strong>on</strong>g>WHO</str<strong>on</strong>g> <str<strong>on</strong>g>m<strong>on</strong>ographs</str<strong>on</strong>g> <strong>on</strong> <strong>selected</strong> <strong>medicinal</strong> <strong>plants</strong><br />

cin-induced gastric ulcerati<strong>on</strong> was reduced in animals treated with 400 mg/<br />

kg bw of the methanol extract (26). Intragastric administrati<strong>on</strong> of an ethanol<br />

extract of the c<strong>ru</strong>de d<strong>ru</strong>g at a dose of 5.0 or 15.0 g/kg bw inhibited<br />

hydrochloric acid-induced gastric ulcerati<strong>on</strong> in mice (27).<br />

Anti-inflammatory activity<br />

Magnolol, isolated and purified from the c<strong>ru</strong>de d<strong>ru</strong>g, inhibited mouse<br />

hind-paw oedema induced by carrageenan, compound 48/80 and polymyxin<br />

B and reversed passive Arthus reacti<strong>on</strong> when administered orally<br />

at a dose of 30 mg/kg bw (28).<br />

Antioxidant activity<br />

The accumulati<strong>on</strong> of oxygen-free radicals and activati<strong>on</strong> of neutrophils<br />

are implicated in the pathophysiological mechanisms that mediate myocardial<br />

ischaemia/reperfusi<strong>on</strong> injury. Thus, antioxidants are purported to<br />

have cardioprotective activity. The antioxidant effect of magnolol was<br />

evaluated in an open-chest anaesthetized rat model of myocardial ischaemia/reperfusi<strong>on</strong><br />

injury (29). Intravenous pretreatment with magnolol, at<br />

a dose of 0.2 and 0.5 μg/kg bw at 10 minutes prior to 45 minutes of left<br />

cor<strong>on</strong>ary artery occlusi<strong>on</strong>, reduced the incidence and durati<strong>on</strong> of ventricular<br />

fibrillati<strong>on</strong> and reduced mortality when compared with the c<strong>on</strong>trol<br />

group. After 1 hour of reperfusi<strong>on</strong>, pretreatment with magnolol reduced<br />

infarct size. In additi<strong>on</strong>, magnolol, at a dose of 0.2 μg/kg bw,<br />

reduced superoxide ani<strong>on</strong> producti<strong>on</strong> and myeloperoxidase activity, an<br />

index of neutrophil infiltrati<strong>on</strong> in the ischaemic myocardium (29).<br />

Restenosis, a comm<strong>on</strong> complicati<strong>on</strong> after ballo<strong>on</strong> angioplasty, involves a<br />

number of cytokines, chemotactic factors and growth factors. Antioxidants<br />

have been shown to inhibit intimal thickening after ballo<strong>on</strong> injury in hyperlipidaemic<br />

animals. The effects of magnolol <strong>on</strong> the expressi<strong>on</strong> of m<strong>on</strong>ocyte<br />

chemotactic protein-1 and <strong>on</strong> intimal resp<strong>on</strong>se in ballo<strong>on</strong>-injured aorta of<br />

cholesterol-fed rabbits were investigated. The animals were fed a 2% highcholesterol<br />

diet together with daily intramuscular injecti<strong>on</strong> of either 1 μg/kg<br />

bw of magnolol or vehicle solvent for a total of 6 weeks, while 10 rabbits fed<br />

a regular diet served as a c<strong>on</strong>trol group. A ballo<strong>on</strong> denudati<strong>on</strong> of abdominal<br />

aorta was performed in each group at the end of the third week, and aortas<br />

were harvested at the end of 6 weeks. Treatment with magnolol significantly<br />

inhibited copper-induced low-density lipoprotein oxidati<strong>on</strong> in cholesterolfed<br />

rabbits and reduced atheroma formati<strong>on</strong> (p < 0.05) in thoracic aortas<br />

without lowering se<strong>ru</strong>m cholesterol. The intimal resp<strong>on</strong>se was significantly<br />

attenuated in magnolol-treated rabbits receiving high cholesterol when compared<br />

to those of the c<strong>on</strong>trol high-cholesterol group (p < 0.05) (30).<br />

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