- Clinical data 90%
- Efficacy 80%
- Security 70%
- Toxicity 30%
No information was found.
The bark is 1–2 cm wide and 1–2 mm thick and occurs in flexible, elongated, quilled or curved pieces. The outer surface is smooth or slightly wrinkled longitudinally and greenish-yellow in the younger bark to brownishgrey in the older bark. The inner surface is smooth or finely striated longitudinally and white, pale yellow or reddish-brown, depending on the species. The fracture is short in the outer part and coarsely fibrous in the inner region, and is easily split longitudinally. The diameter of current year twigs is not more than 10 mm. The wood is white or pale yellow.
Major chemical constituents
The major biologically active constituents are the phenolic glycosides including salicin (approximately 1%), salicortin (up to 4.0%), 2´ Oacetylsalicortin (up to 10%), 2´-O-acetylsalicin (= fragilin, up to 4%), tremulacin (0.12–2%), 3´- and 4´-acetylsalicortin, populin and salireposide, which have collectively been designated as “salicylates”. Triandrin, vimalin, picein and grandidentatin are non-saligenin structure-based phenolic compounds. Other significant constituents are flavonoids and tannins. Total salicin content (after hydrolysis) varies according to species. Species rich in total salicin include S. daphnoides (2–10%), S. purpurea (4–8.5%), S. fragilis (2–10%) and S. alba (0.5–1%).
Medicinal uses of Salix alba
Uses supported by clinical data
Salix alba used orally for the symptomatic treatment of fever and pain, and symptomatic treatment of mild rheumatic conditions.
Uses described in pharmacopoeias and well established documents
Used orally for the treatment of the common cold.
Uses described in traditional medicine
Used orally for the treatment of constipation and urinary incontinence.
Used externally for the treatment of warts.
Similar to salicylates, such as acetylsalicylic acid, extracts of the crude drug are thought to act by inhibiting the activity of cyclooxygenase and thereby inhibiting the synthesis of prostaglandins, which play a role in inflammation, fever and pain. Acetylsalicylic acid inhibits the synthesis of prostaglandins through the acetylation of the enzyme cyclooxygenase. Salicylic acid, and the salicylates that lack an acetyl group, reduce prostaglandin synthesis via inhibition of the activity of cyclooxygenase II. Intragastric administration of 100.0 mg/kg body weight (bw) of tremulacin, a constituent of the bark, significantly inhibited carrageenaninduced hind paw oedema in rats (p < 0.001). Intragastric administration of 0.5 ml/kg bw of a 30% ethanol extract of the bark to rats reduced carrageenan-induced hind paw oedema, but was not effective in the adjuvant- induced arthritis or dextran-induced pedal oedema models.
Intragastric administration of 0.8 ml/kg bw of a 30% ethanol extract to rats, suppressed yeast-induced pyrexia. The antipyretic effects of salicin, saligenin (an aglycone of salicin) and salicylic acid (an active metabolite of salicin) were assessed in rats. After intragastric administration of salicin to rats, the metabolite salicylic acid appeared slowly in the plasma and concentrations increased gradually, in contrast to the rapid appearance observed after oral administration of sodium salicylate or saligenin. At a dose of 5 mM/kg bw, orally administered salicin did not affect the rectal temperature of afebrile rats while at the same dose, sodium salicylate and saligenin lowered body temperature significantly. However, salicin significantly reduced yeast-induced fever (p < 0.01), producing a normal body temperature, and completely prevented fever when administered simultaneously with yeast. Salicin did not induce gastric lesions even at a dose of 5 mM/kg bw; conversely, sodium salicylate and saligenin induced severe gastric lesions in a dose-dependent manner when administered at doses of 1, 2.5 and 5 mM/kg bw.
The pharmacokinetics of salicin, saligenin (an aglycone of salicin) and salicylic acid (an active metabolite of salicin) were determined in rats. Poor absorption of salicin and rapid absorption of salicylic acid and saligenin were confirmed in this animal model. Only small amounts of salicylic acid and saligenin were detected in the intestinal tracts of rats 1 h after oral administration. More than 50% of a salicin dose was recovered as salicin and saligenin from the intestinal tracts 1 h after treatment and 15.8% of the dose was still present as saligenin 4 h after administration.
When given to germ-free rats, 19.8% of the salicin dose was recovered intact, mainly from the cecum, and no saligenin was detected even at 4 h after treatment. These results indicate that salicin is a pro-drug that is gradually transported to the lower part of the intestine, hydrolysed to saligenin by intestinal bacteria, and converted to salicylic acid after absorption. It thus produces an antipyretic action without causing gastric injury.
A study was performed to investigate the anticoagulant activity of a bark extract used in the treatment of 51 patients with chronic back pain. Thirty-five patients suffering from acute exacerbations of chronic low back pain received randomly and double-blind either the extract (corresponding to 240 mg salicin/day; n = 19) or a placebo (n = 16). A further 16 patients with stable chronic ischaemic heart disease were given 100 mg acetylsalicylate per day. Platelet aggregation was studied after drawing blood from the treated patients using an aggregometer. Arachidonic acid (500 μg/ml), adenosine diphosphate (2 × 10−5 M) and collagen (0.18 μg/ml) were used as aggregating agents. The mean maximal arachidonic acid-induced platelet aggregation was 61%, 78% and 13% for the groups treated with extract, placebo and acetylsalicylate, respectively. Acetylsalicylate had a significant inhibitory effect on platelet aggregation compared to the extract (p = 0.001) and placebo (p = 0.001). There was also a significant difference between the placebo and the extract-treated groups in the maximal platelet aggregation induced by arachidonic acid (p = 0.04) and ADP (p = 0.01). No statistical difference was found between platelet aggregation in the three groups when collagen was added to the human platelets. Daily consumption of the extract with 240.0 mg salicin per day affected platelet aggregation to a lesser extent than acetylsalicylate.
Cortex Salicis is contraindicated in cases of hypersensitivity or allergy to the plant material or to salicylates (e.g. asthma, bronchial spasm, rhinitis or urticaria).
It is also contraindicated during pregnancy and lactation, in patients with salicylate intolerance and patients with impaired thrombocyte function, and in children under the age of 12 years.
In children under the age of 12 years, Cortex Salicis should only be used on the advice of a health care professional due to the possibility of Reye’s syndrome. In cases of a child or adolescent who has become very ill with severe vomiting, drowsiness or loss of consciousness following a viral infection, Reye’s syndrome should be suspected. This extremely rare, lifethreatening disease requires immediate medical attention. In cases of severe liver or renal dysfunction, coagulation disorders, gastric/duodenal ulcer and glucose-6-phosphate dehydrogenase deficiency, the product should only be taken under medical supervision. Consult a health care professional in cases of fever (> 39 C), lasting longer than 3 days. A health care professional should also be consulted if acute conditions of swelling of joints, redness and impaired mobility persist or worsen during the first week of use of Cortex Salicis.
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