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Folium Sennae Definition Folium Sennae consists of the dried leaflets ofCassia senna L. (Fabaceae).1 1C. italica Mill. is listed in the Malian pharmacopoeia. Synonyms Fabaceae are also referred to as Leguminosae. Although recognized as two distinct species in many pharmacopoeias (1–8), Cassia acutifolia Delile and C. angustifolia Vahl. are considered botanically to be synonyms of the single species Cassia senna L. (9). Selected vernacular names Alexandria senna, Alexandrian senna, cassia, eshrid, falajin, fan xie ye, filaskon maka, hindisana, illesko, Indian senna, ma khaam khaek, makhaam khaek, mecca senna, msahala, nelaponna, nelatangedu, nilavaka, nilavirai, nubia senna, rinji, sanai, sand hijazi, sanjerehi, sen de alejandria, sen de la india, senna makki, senna, senamikki, sennae folium, sona-mukhi, Tinnevelly senna, true senna (3, 10–14). Description Low shrubs, up to 1.5 m high, with compound paripinnate leaves, having 3–7 pairs of leaflets, narrow or rounded, pale green to yellowish green. Flowers, tetracyclic, pentamerous, and zygomorphic, have quincuncial calyx, a corolla of yellow petals with brown veins, imbricate ascendent prefloration, and a partially staminodial androeceum. The fruit is a broadly elliptical, somewhat reniform, flattened, parchment-like, dehiscent pod, 4–7 cm long by 2 cm wide, with 6 to 10 seeds (11, 14, 15). Plant material of interest: leaflets General appearance Macroscopically, the leaflets are lanceolate or lanceolate-ovate, unequal at the base, with entire margin, acute-mucronate apex and short, stout petioles; sometimes broken; 1.5–5cm in length and 0.5–1.5cm in width, bearing a fine pubescence of appressed hairs, more numerous on the lower surface (1–7). Organoleptic properties The colour is weak yellow to pale olive (1, 2). The odour is characteristic, and the taste is mucilage-like and then slightly bitter (1, 3). Microscopic characteristics Epidermis with polygonal cells containing mucilage; unicellular thick-walled trichomes, length, up to 260µm, slightly curved at the base, warty; paracytic stomata on both surfaces; under the epidermal cells a single row of palisade layer; cluster crystals of calcium oxalate distributed throughout the lacunose tissue; on the adaxial surface, sclerenchymatous fibres and a gutter-shaped group of similar fibres on the abaxial side containing prismatic crystals of calcium oxalate (1). Powdered plant material Light green to greenish yellow. Polygonal epidermal cells showing paracytic stomata. Unicellular trichomes, conical in shape, with warty walls, isolated or attached to fragments of epidermis. Fragments of fibrovascular bundles with a crystal sheath containing calcium oxalate prisms. Cluster crystals isolated or in fragments of parenchyma (2, 3). Geographical distribution The plant is indigenous to tropical Africa. It grows wild near the Nile river from Aswan to Kordofan, and in the Arabian peninsula, India and Somalia (15). It is cultivated in India, Pakistan, and the Sudan (11, 12, 14, 15). General identity tests Macroscopic, microscopic examinations, and microchemical analysis (1–6), and thin-layer chromatographic analysis for the presence of characteristic sennosides (sennosides A–D) (3–5). Purity tests Microbiology The test for Salmonella spp. in Folium Sennae products should be negative. The maximum acceptable limits of other microorganisms are as follows (16–18). For preparation of decoction: aerobic bacteria-107/g; moulds and yeast-105/g; Escherichia coli-102/g; other enterobacteria-104/g. Preparations for internal use: aerobic bacteria-105/g; moulds and yeast-104/g; Escherichia coli-0/g; other enterobacteria-103/g. Foreign organic matter Not more than 2.0% of stems (1) and not more than 1.0% of other foreign organic matter (1, 4, 8). Total ash Not more than 12% (5). Acid-insoluble ash Not more than 2.0% (1, 8). Water-soluble extractive Not less than 3% (1). Moisture Not more than 10% (6). Pesticide residues To be established in accordance with national requirements. Normally, the maximum residue limit of aldrin and dieldrin in Folium Sennae is not more than 0.05 mg/kg (18). For other pesticides, see WHO guidelines on quality control methods for medicinal plants (16) and guidelines for predicting dietary intake of pesticide residues (19). Heavy metals Recommended lead and cadmium levels are not more than 10 and 0.3mg/kg, respectively, in the final dosage form of the plant material (16). Radioactive residues For analysis of strontium-90, iodine-131, caesium-134, caesium-137, and plutonium-239, see WHO guidelines on quality control methods for medicinal plants (16). Other purity tests Chemical tests and tests of alcohol-soluble extractive are to be established in accordance with national requirements. Chemical assays Contains not less than 2.5% of hydroxyanthracene glycosides, calculated as sennoside B (1, 4, 5).Quantitative analysis is performed by spectrophotometry (1, 4–8) and by high-performance liquid chromatography (20). Thin-layer chromatography is employed for qualitative analysis for the presence of sennosides A and B (3–5). Major chemical constituents Folium Sennae contains a family of hydroxyanthracene glycosides, the most plentiful of which are sennosides A and B. There are also small amounts of aloeemodin and rhein 8-glucosides, mucilage, flavonoids, and naphthalene precursors (15). 
Dosage forms Crude plant material, powder, oral infusion, and extracts (liquid or solid) standardized for content of sennosides A and B (15, 21, 22). Package in well-closed containers protected from light and moisture (1–8). Medicinal uses Uses supported by clinical data Short-term use in occasional constipation (21–25). Uses described in pharmacopoeias and in traditional systems of medicine None. Uses described in folk medicine, not supported by experimental or clinical data As an expectorant, a wound dressing, an antidysenteric, and a carminative agent; and for the treatment of gonorrhoea, skin diseases, dyspepsia, fever, and haemorrhoids (11, 23, 25). Pharmacology Experimental pharmacology The effects of Folium Sennae are due primarily to the hydroxyanthracene glucosides, especially sennosides A and B. These β-linked glucosides are secretagogues that increase net secretion of fluids and specifically influence colonic motility and enhance colonic transit. They are not absorbed in the upper intestinal tract; they are converted by the bacteria of the large intestine into the active derivatives (rhein-anthrone). The mechanism of action is twofold: (1) effect on the motility of the large intestine (stimulation of peristaltic contractions and inhibition of local contractions), resulting in an accelerated colonic transit, thereby reducing fluid absorption, and (2) an influence on fluid and electrolyte absorption and secretion by the colon (stimulation of mucus and active chloride secretion), increasing fluid secretion (24, 25). Clinical pharmacology The time of action of senna is usually 8–10 hours, and thus the dose should be taken at night (24). The action of the sennosides augments, without disrupting, the response to the physiological stimuli of food and physical activity (24). The sennosides abolish the severe constipation of patients suffering from severe irritable bowel syndrome (26). In therapeutic doses, the sennosides do not disrupt the usual pattern of defecation times and markedly soften the stool (24). Sennosides significantly increase the rate of colonic transit (27) and increase colonic peristalsis, which in turn increase both faecal weight and dry bacterial mass (24, 28). Due to their colonic specificity, the sennosides are poorly absorbed in the upper gastrointestinal tract (29). Toxicity The major symptoms of overdose are griping and severe diarrhoea with consequent losses of fluid and electrolytes. Treatment should be supportive with generous amounts of fluid. Electrolytes, particularly potassium, should be monitored, especially in children and the elderly. Contraindications As with other stimulant laxatives, the drug is contraindicated in persons with ileus, intestinal obstruction, and stenosis, atony, undiagnosed abdominal symptoms, inflammatory colonopathies, appendicitis, abdominal pains of unknown cause, severe dehydration states with water and electrolyte depletion, or chronic constipation (21, 30). Folium Sennae should not be used in children under the age of 10 years. Warnings Stimulant laxative products should not be used when abdominal pain, nausea, or vomiting are present. Rectal bleeding or failure to have a bowel movement after use of a laxative may indicate a serious condition (31). Chronic abuse, with diarrhoea and consequent fluid electrolyte losses, may cause dependence and need for increased dosages, disturbance of the water and electrolyte balance (e.g. hypokalaemia), atonic colon with impaired function, albuminuria and haematuria (29, 32). The use of stimulant laxatives for more than 2 weeks requires medical supervision. Chronic use may lead to pseudomelanosis coli (harmless). Hypokalaemia may result in cardiac and neuromuscular dysfunction, especially if cardiac glycosides (digoxin), diuretics, corticosteroids, or liquorice root are taken (29). Precautions General Use for more than 2 weeks requires medical attention (21, 31). Drug interactions Decreased intestinal transit time may reduce absorption of orally administered drugs (32, 33). The increased loss of potassium may potentiate the effects of cardiotonic glycosides (digitalis, strophanthus). Existing hypokalaemia resulting from longterm laxative abuse can also potentiate the effects of antiarrhythmic drugs, such as quinidine, which affect potassium channels to change sinus rhythm. Simultaneous use with other drugs or herbs which induce hypokalaemia, such as thiazide diuretics, adrenocorticosteroids, or liquorice root, may exacerbate electrolyte imbalance (21, 22). Drug and laboratory test interactions Urine discoloration by anthranoid metabolites may lead to false positive test results for urinary urobilinogen, and for estrogens measured by the Kober procedure (32). Carcinogenesis, mutagenesis, impairment of fertility No in vivo genotoxic effects have been reported to date (34–37). Although chronic abuse of anthranoid-containing laxatives was hypothesized to play a role in colorectal cancer, no causal relationship between anthranoid laxative abuse and colorectal cancer has been demonstrated (38–40). Pregnancy: non-teratogenic effects Use during pregnancy should be limited to conditions in which changes in diet or fibre laxatives are not effective (41). Nursing mothers Use during breast-feeding is not recommended owing to insufficient data on the excretion of metabolites in breast milk (21). Small amounts of active metabolites (rhein) are excreted into breast milk, but a laxative effect in breast-fed babies has not been reported (21). Paediatric use Contraindicated for children under 10 years of age (21). Other precautions No information available on teratogenic effects in pregnancy. Adverse reactions Senna may cause mild abdominal discomfort such as colic or cramps (21, 22, 33). A single case of hepatitis has been described after chronic abuse (42). Melanosis coli, a condition which is characterized by pigment-loaded macrophages within the submucosa, may occur after long-term use. This condition is clinically harmless and disappears with cessation of treatment (33, 43, 44). Long-term laxative abuse may lead to electrolyte disturbances (hypokalaemia, hypocalcaemia), metabolic acidosis or alkalosis, malabsorption, weight loss, albuminuria, and haematuria (21, 22,33). Weakness and orthostatic hypotension may be exacerbated in elderly patients when stimulant laxatives are repeatedly used (21, 33). Conflicting data exist on other toxic effects such as intestinal-neuronal damage due to long-term misuse (45–54). Posology The correct individual dose is the smallest required to produce a comfortable, soft-formed motion (21). Powder: 1–2g of leaf daily at bedtime (11). Adults and children over 10 years: standardized daily dose equivalent to 10–30mg sennosides (calculated as sennoside B) taken at night. References 1. The international pharmacopoeia, 3rd ed. Vol. 3. Quality specifications. Geneva, World Health Organization, 1988. 2. The United States Pharmacopeia XXIII. Rockville, MD, US Pharmacopeial Convention, 1996. 3. African pharmacopoeia, 1st ed. Lagos, Organization of African Unity, Scientific, Technical & Research Commission, 1985. 4. British pharmacopoeia. London, Her Majesty's Stationery Office, 1988. 5. European pharmacopoeia, 2nd ed. Strasbourg, Council of Europe, 1995. 6. Pharmacopoeia of the People's Republic of China (English ed.). Guangzhou, Guangdong Science and Technology Press, 1992. 7. Deutsches Arzneibuch 1996. Stuttgart, Deutscher Apotheker Verlag, 1996. 8. Pharmacopée française. Paris, Adrapharm, 1996. 9. Brenan JPM. New and noteworthy Cassia from tropical Africa. Kew bulletin, 1958, 13:231–252. 10. Farnsworth NR, ed. NAPRALERT database. Chicago, University of Illinois at Chicago, IL, March 15, 1995 production (an on-line database available directly through the University of Illinois at Chicago or through the Scientific and Technical Network (STN) of Chemical Abstracts Services). 11. Youngken HW. Textbook of pharmacognosy, 6th ed. Philadelphia, Blakiston, 1950. 12. Medicinal plants of India, Vol. 1. New Delhi, Indian Council of Medical Research, 1976. 13. Huang KC. The pharmacology of Chinese herbs. Boca Raton, FL, CRC Press, 1994. 14. Farnsworth NR, Bunyapraphatsara N, eds. Thai medicinal plants. Bangkok, Prachachon, 1992. 15. Bruneton J. Pharmacognosy, phytochemistry, medicinal plants. Paris, Lavoisier, 1995. 16. Quality control methods for medicinal plant materials. Geneva, World Health Organization, 1998. 17. Deutsches Arzneibuch 1996. Vol. 2. Methoden der Biologie. Stuttgart, Deutscher Apotheker Verlag, 1996. 18. European pharmacopoeia, 3rd ed. Strasbourg, Council of Europe, 1997. 19. Guidelines for predicting dietary intake of pesticide residues, 2nd rev. ed. Geneva. World Health Organization, 1997 (unpublished document WHO/FSF/FOS/97.7; available from Food Safety, WHO, 1211 Geneva 27, Switzerland). 20. Duez P et al. Comparison between high-performance thin-layer chromatography- fluorometry and high-performance liquid chromatography for the determination of sennosides A and B in Senna (Cassia spp.) pods and leaves. Journal of chromatography, 1984, 303:391–395. 21. Core-SPC for Sennae Folium. Coordinated review of monographs on herbal remedies. Brussels, European Commission, 1994. 22. German Commission E Monograph, Senna folium. Bundesanzeiger, 1993, 133:21 July. 23. Leng-Peschlow E. Dual effect of orally administered sennosides on large intestine transit and fluid absorption in the rat. Journal of pharmacy and pharmacology, 1986, 38:606–610. 24. Godding EW. Laxatives and the special role of Senna. Pharmacology, 1988, 36(Suppl. 1):230–236. 25. Bradley PR, ed. British herbal compendium, Vol. 1. Bournemouth, British Herbal Medicine Association, 1992. 26. Waller SL, Misiewicz JJ. Prognosis in the irritable-bowel syndrome. Lancet, 1969, ii:753–756. 27. Ewe K, Ueberschaer B, Press AG. Influence of senna, fibre, and fibre + senna on colonic transit in loperamide-induced constipation. Pharmacology, 47(Suppl. 1):242– 248. 28. Stephen AM, Wiggins HS, Cummings JH. Effect of changing transit time on colonic microbial metabolism in man. Gut, 1987, 28:610. 29. Goodman and Gilman's the pharmacological basis of therapeutics, 9th ed. New York, McGraw-Hill, 1996. 30. Physicians' desk reference, 49th ed. Montvale, NJ, Medical Economics Company, 1995. 31. American hospital formulary service. Bethesda, MD, American Society of Hospital Pharmacists, 1990. 32. United States pharmacopeia, drug information. Rockville, MD, US Pharmacopeial Convention, 1992. 33. Martindale, the extra pharmacopoeia, 30th ed. London, Pharmaceutical Press, 1993. 34. Heidemann A, Miltenburger HG, Mengs U. The genotoxicity of Senna. Pharmacology, 1993, 47(Suppl. 1):178–186. 35. Tikkanen L et al. Mutagenicity of anthraquinones in the Salmonella preincubation test. Mutation research, 1983, 116:297–304. 36. Westendorf et al. Mutagenicity of naturally occurring hydroxyanthraquinones. Mutation research, 1990, 240:1–12. 37. Sanders D et al. Mutagenicity of crude Senna and Senna glycosides in Salmonella typhimurium.Pharmacology and toxicology, 1992, 71:165–172. 38. Lyden-Sokolowsky A, Nilsson A, Sjoberg P. Two-year carcinogenicity study with sennosides in the rat: emphasis on gastrointestinal alterations. Pharmacology, 1993, 47(Suppl. 1):209–215. 39. Kune GA. Laxative use not a risk for colorectal cancer: data from the Melbourne colorectal cancer study. Zeitschrift für Gasteroenterologie, 1993, 31:140–143. 40. Siegers CP. Anthranoid laxatives and colorectal cancer. Trends in pharmacological sciences, 1992, 13:229–231. 41. Lewis JH et al. The use of gastrointestinal drugs during pregnancy and lactation. American journal of gastroenterology, 1985, 80:912–923. 42. Beuers U, Spengler U, Pape GR. Hepatitis after chronic abuse of Senna. Lancet, 1991, 337:472. 43. Loew D. Pseudomelanosis coli durch Anthranoide. Zeitschrift für Phytotherapie, 1994, 16:312–318. 44. Müller-Lissner SA. Adverse effects of laxatives: facts and fiction. Pharmacology, 1993, 47(Suppl. 1):138–145. 45. Godding EW. Therapeutics of laxative agents with special reference to the anthraquinones.Pharmacology, 1976, 14(Suppl. 1):78–101. 46. Dufour P, Gendre P. Ultrastructure of mouse intestinal mucosa and changes observed after long term anthraquinone administration. Gut, 1984, 25:1358–1363. 47. Dufour P et al. Tolérance de la muqueuse intestinale de la souris à l'ingestion prolongée d'une poudre de sené. Annales pharmaceutiques françaises, 1983, 41(6):571– 578. 48. Kienan JA, Heinicke EA. Sennosides do not kill myenteric neurons in the colon of the rat or mouse. Neurosciences, 1989, 30(3):837–842. 49. Riemann JF et al. Ultrastructural changes of colonic mucosa in patients with chronic laxative misuse. Acta hepato-gastroenterology, 1978, 25:213–218. 50. Smith BA. Effect of irritant purgatives on the myenteric plexus in man and the mouse. Gut, 1968, 9:139–143. 51. Riemann JF et al. The fine structure of colonic submucosal nerves in patients with chronic laxative abuse. Scandinavian journal of gastroenterology, 1980, 15:761–768. 52. Rieken EO et al. The effect of an anthraquinone laxative on colonic nerve tissue: a controlled trial in constipated women. Zeitschrift für Gasteroenterologie, 1990, 28:660– 664. 53. Riemann JF, Schmidt H. Ultrastructural changes in the gut autonomic nervous system following laxative abuse and in other conditions. Scandinavian journal of gastroenterology, 1982, 71(Suppl.):111–124. 54. Krishnamurti S et al. Severe idiopathic constipation is associated with a distinctive abnormality of the colonic myenteric plexus. Gastroenterology, 1985, 88:26–34. |
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