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At least 19 recordsLinked to original sources
PubMed2001

Apoptosis induction by sennoside laxatives in man; escape from a protective mechanism during chronic sennoside use?

Chronic sennoside use induces melanosis coli (MC) and possibly increases colorectal cancer risk. Sennosides alter colonic crypt length, proliferative activity, and bcl-2 expression 18 h after administration. To investigate possible mechanisms for carcinogenesis, the effects of acute sennoside use and the presence of MC on colorectal epithelium were studied. Colorectal biopsies from 15 subjects receiving sennosides 6 h before sigmoidoscopy (Sen), 15 controls (NSen), and 27 with MC [11 moderate (MMC) and 16 severe (SMC)]. were analysed for degree of apoptosis (H&E staining), immunohistochemical p53, p21/WAF and bcl-2 expression, and proliferative activity (labelling index, LI). Apoptosis (p=0.0004), intensity of p53 staining (p=0.01), and p21/WAF expression (p=0.008) were increased in Sen and SMC compared with NSen and MMC. p53 expression was increased in Sen (p=0.004). No difference in bcl-2 expression or LI was observed. Crypts were shorter in Sen (p=0.05) and longer in SMC (p=0.04) than in NSen. It is concluded that sennosides acutely induce apoptosis of colonic epithelial cells, presumably by a p53, p21/WAF-mediated pathway, resulting in shorter crypts. In severe melanosis coli, apoptosis seems to be delayed, causing longer crypts without a rise in proliferative activity or bcl-2 expression. This escape from a presumably protective mechanism may enhance the risk of carcinogenesis during chronic sennoside use.

Adolescent↗
PubMed1999

[Determination of sennoside A and sennoside B in formulation using capillary electrophoresis].

The determination of sennoside A (SA) and sennoside B (SB) by capillary zone electrophoresis was developed. The separation of SA and SB was performed in 100 mM of the 3-[cyclohexylamino]-1-propanesulfonic acid (CAPS) buffer (pH 10.0), and the migration time of SA and SB was found to be both less than 7 min. This method was applied to the analyses of seven commercial formulations containing SA and SB without previous treatment. The statistical comparison of the results obtained from both capillary electrophoresis and HPLC methods revealed an absolute correlation.

Anthraquinones↗
PubMed1996

[Sennosides Reference Standard (Control 951) of the National Institute of Health Sciences].

The "Sennosides Reference Standard (Control 951)" was prepared, which is intended to be used for the fluorophotometric assay of sennosides content in the preparation of "Sennosides". In this assay hydroxylated mono- and dianthraquinone glucosides are chelated with boric acid, and the fluorescence intensity of the chelate is determined against that of the Reference Standard (RS). In the establishment of this RS, sennosides content in the candidate material must be determined accurately by fluorophotometry. The Sennoside AB for assay, prepared as an equimolar mixture of the purified sennoside A and Sennoside B, was used as the RS for the fluorophotometry. Based on the above concept, sennosides content in the candidate was determined as calcium salts to be 60.1 +/- 1.6% by the fluorophotometry. Thus the sennosides content of this Sennosides RS was certified to be 60%. Separately, contents of Sennoside A (SA) and Sennoside B (SB) in this candidate were determined by using HPLC. As a result, the sum of SA and SB was estimated to be 38% as free acids. Thus it was suggested that about 20% of dianthraquinone glucosides other than SA and SB and anthraquinone glucosides may be included in this Sennoside RS as free acids. Analytical results on the USP Sennosides RS were also shown and discussed, compared with the present Sennosides RS.

Anthraquinones↗
PubMed1988

New aspects on the metabolism of the sennosides.

Pure sennoside B was administered to rats. On appearance of the first wet faeces, sennoside B and its metabolites were determined in different parts of the alimentary tract, in faeces and in the urine. The total recovery of unchanged sennoside B and its metabolites was determined by alkali fusion followed by colorimetry and high-pressure liquid chromatography (HPLC). Alkali fusion in 1 N sodium hydroxide solution formed red solutions with sennosides and sennoside derivatives. The molar absorbance of sennosides A and B, sennidin B monoglucoside, sennidins, rhein, danthron, dithranol, rhein-8-glucoside and rhein anthrone at wavelengths of 505-530 nm related approximately to the number of ionizable hydroxy groups in the molecule. Brown polymerized products were isolated from the senna drug. The colour intensity of these products was approximately the same by weight as that of the sennosides themselves, although sennidins could no longer be freed from these by acid hydrolysis. After administration of sennoside B, the average sum of unchanged glucoside and known metabolites in different parts of the gastrointestinal tract and faeces of rats was 61.6% according to HPLC and 92.8% according to the alkali fusion procedure. This difference is indicative of the presence of substances which are no longer identifiable as sennoside derivatives, either by HPLC or by other classical chromatographic methods. Sennosides seem to be partly present in the alimentary tract in polymerized or bound form. The alkali fusion method may be useful in connection with the isolation of as yet unknown metabolites of the sennosides in the gastrointestinal tract.

Alkalies↗
PubMed2000

Estimation of individual sennosides in plant materials and marketed formulations by an HPTLC method.

Senna is a well-known drug, used in the Ayurvedic and Allopathic systems of medicine, and is a treatment for constipation. The purgative action of senna and its formulations is due to the presence of sennosides A and B. An HPTLC method has been developed for the determination of individual sennosides (A, B, C, D) without any derivatization in marketed formulations (three tablet formulations, two granule formulations and one liquid formulation) and plant materials (senna leaf and pod). The methanolic solution of a sample was applied on a pre-coated silica gel G60 F254 TLC plate (E. Merck.) and was developed using n-propanol : ethyl acetate : water : glacial acetic acid (3 : 3 : 2 : 0.1 v/v) as the mobile phase. The relative band speeds (Rf values) obtained were 0.35, 0.25, 0.61, 0.46 for sennosides A, B, C and D, respectively. The densitometric response was monitored at 366nm. Calibration curves were found to be linear in the concentration ranges 193-1356, 402-2817, 71-497 and 132-927 ng per spot for sennosides A, B, C, and D, respectively. The correlation coefficients were found to be 0.9978, 0.9987, 0.9939 and 0.9983 respectively for sennosides A, B, C and D. The result obtained with the HPTLC method for total sennoside content was compared with the results using the pharmacopoeial methods (spectrophotometric (British Pharmacopoeia) and spectrofluorimetric (United States Pharmacopeia) using the 'F' test). The results revealed no significant difference in the three different methods for estimation of total sennoside. The proposed HPTLC method was found to be simple, specific, precise, accurate and rapid. It can be used for routine quality control of sennosides or senna-containing formulations for individual sennosides.

Anthraquinones↗
PubMed1996

A sennoside-hydrolyzing beta-glucosidase from Bifidobacterium sp. strain SEN is inducible.

Bifidobacterium sp. strain SEN was isolated and characterized by hydrolytic conversion of sennosides to sennidins (Akao et al., Appl. Environ. Microbiol., 60, 1041 (1994)). The sennoside-hydrolyzing capacity of the strain SEN was disappeared following the addition of glucose to the media in spite of good bacterial growth and potent activity hydrolyzing p-nitrophenyl beta-D-glucopyranoside (pNPG). In a fructose-containing medium, no such suppressing effect was shown. Following a 10 h incubation in 50 mM potassium phosphate buffer (pH 7.4), the sennoside-hydrolyzing activity of the bacterium increased, dose-dependently, with the addition of sennoside B. Inhibition of the substrate-induced increase in sennoside-hydrolyzing activity was observed following the addition of some antibiotics (chloramphenicol, streptomycin, and rifampicin). In particular, chloramphenicol completely inhibited the increase of sennoside-hydrolyzing activity while 38% pNPG-hydrolyzing activity remained. It is suggested that the strain SEN produces two different beta-glucosidases of which the sennoside-hydrolyzing enzyme is inducible. In addition, the glucosides pNPG, esculin, salicin, or amygdalin stimulated the induction of the sennoside beta-glucosidase, but less markedly than sennoside. Sennidin A or sugars (glucose, fructose, cellobiose, or maltose) did not induce the enzyme.

Anthraquinones↗
PubMed2001

[Origin of sennosides in health teas including Malva leaves].

The aim of this study is to clarify whether sennosides are contained in the leaf of Malva verticillata L., and then to clarify the source of sennosides in health teas including malva leaves. The identification and determination of sennosides were performed with thin layer chromatography and high performance liquid chromatography. The leaf of Malva verticillata L. did not contain sennosides A or B and could be easily distinguished from senna leaf. Our previous report showed that sennosides are contained in weight-reducing herbal teas including malva leaves, and that senna leaf is a herbal component in some teas. Furthermore, in 10 samples of health tea including malva leaves that were bought last year, the smallest amount of sennosides was 6.1 mg/bag, and all health teas including malva leaves contained the leaf and midrib of senna. We suggest that sennosides A and B are not contained in the leaf of Malva verticillata L., and that the sennosides in health teas including malva leaves are not derived from malva leaf but from senna leaf.

Anthraquinones↗
PubMed1988

Changes in colonic motility induced by sennosides in dogs: evidence of a prostaglandin mediation.

The effects of sennosides on colonic motility were investigated in eight conscious dogs chronically fitted with two strain gauge transducers in the proximal colon, an intracolonic silicone catheter and a polyethylene catheter implanted in a branch of the right colonic artery. Oral sennosides (30 mg/kg) inhibited colonic motility for 12 to 18 h after a three to six hours delay, and associated with giant contractions and diarrhoea. The minimal oral dose of sennosides to produce such changes varied from 5 to 15 mg/kg. Intracolonic sennosides at the minimal effective dose and at 30 mg/kg reproduced the effects of oral sennosides, but with a shorter latency (0.5-1.5 h). Intracolonic PGE2 (100 micrograms/kg) in viscous gel medium or intra-arterial PGE2 (10 micrograms/h) inhibited colonic motility and induced giant contractions often associated with defecation. The colonic motor changes induced by intracolonic sennosides at the minimal effective dose, but not those induced by intracolonic PGE2, were blocked by intra-arterial indomethacin (10 micrograms/h) or piroxicam (5 micrograms/h). These results suggest that colonic motor actions of sennosides are mediated through a local prostaglandins synthesis, as they were blocked by cyclooxygenase inhibitor and reproduced by PGE2.

Animals↗
PubMed2001

Production of monoclonal antibodies against a major purgative component, sennoside B, their characterization and use in ELISA.

For immunization, sennoside B was conjugated with bovine serum albumin. The hapten density in the antigen conjugate was determined to be 3 mol mol(-1) protein by matrix-assisted laser desorption-ionization TOF mass spectrometry. A hybridoma secreting monoclonal antibody against sennoside B was produced by fusing splenocytes from mouse immunized with the sennoside B conjugate and mouse myeloma cells. Weak cross-reactivities occurred with sennoside A which is a stereochemical isomer, and a monomer of sennoside B, rhein, but no cross-reactivity was observed with other related anthraquinones and phenolics. The range of the assay extended from 0.5 ng ml(-1) to 15 ng ml(-1) of sennoside B, and good correlation between ELISA and HPLC methods was obtained when crude extracts of rhubarb were analyzed.

Anthraquinones↗
PubMed1993

Serotonin antagonists inhibit sennoside-induced fluid secretion and diarrhea.

The aim of this study was to investigate whether 5-hydroxytryptamine (serotonin, 5-HT) is involved in the mediation of sennoside-induced colonic fluid secretion and diarrhea. Oral administration of purified sennosides (25, 40 and 64 mg/kg) dose-dependently reversed net fluid absorption to net fluid secretion, enhanced the incidence of diarrhea and stimulated the release of 5-HT into the colonic lumen from 7.1 to 17.3 ng/g wet weight. The 5-HT2 antagonist ketanserin and the 5-HT3 antagonist tropisetron dose-dependently but only partially reduced sennoside (40 mg/kg)-induced fluid secretion whereas the 5-HT3 antagonist granisetron dose-dependently reduced and at 300 micrograms/kg totally abolished sennoside-induced secretion. Granisetron, but not ketanserin and tropisetron, reduced the incidence of diarrhea in sennoside-treated rats, indicating the involvement of 5-HT also in acceleration of large intestinal transit. It is concluded that 5-HT is an important mediator both of sennoside-induced fluid secretion in the rat colon and of diarrhea.

Animals↗
PubMed1986

Acceleration of large intestine transit time in rats by sennosides and related compounds.

Sennosides A + B and their natural metabolites, sennidins A + B, rheinanthrone and rhein, as well as the synthetic laxative danthron, were investigated for their influence on small and large intestine transit time in rats. Carmine red, as a marker, was administered through a gastric tube for small intestine transit or intracaecally by a chronically implanted catheter for colon transit. High doses of sennosides (250-500 mg kg-1) given orally from 20 min or up to 6 h before marker administration had no effect on small intestine transit time. The metabolites and danthron (10-100 mg kg-1 p.o.) also did not accelerate upper gastrointestinal passage. Intracaecal administration at the same time as carmine red, however, reduced the time for the appearance of the first coloured faeces from more than 8 h in the controls to 46 +/- 9 min after sennosides, 34 +/- 11 min after sennidins, 53 +/- 83 min after rhein and 16 +/- 4 min after rheinanthrone (50 mg kg-1 of each). Danthron was ineffective. Thus, sennosides and their natural metabolites specifically influence large intestinal motility. Acceleration of colonic transport seems to be a major component of the laxative action whereas for danthron motility changes are not responsible for its laxative action. Indomethacin partly inhibited the acceleration of large intestine transit induced by sennosides. An involvement of endogenous prostaglandins may therefore be possible, although a local bolus administration of PGF2 alpha or PGE2 into the caecal lumen neither influenced transit time nor induced diarrhoea.

Animals↗
PubMed1993

Sennoside-induced secretion is not caused by changes in mucosal permeability or Na+,K(+)-ATPase activity.

The effect of sennosides (50 mg kg-1) on the rat colon in-situ was studied 6 h after oral treatment when the laxative effect was maximal. In a second experiment, rhein (4 x 10(-3) M), an active sennoside metabolite, was administered into the lumen of the colon for 1 h. Both sennosides and rhein reduced net H2O and Na+ absorption or reversed it to net secretion. Paracellular permeability, as measured using erythritol as a small marker molecule, was increased 2- to 3-fold; permeability to a large molecule, PEG 1000, was unchanged. The activity of Na+,K(+)-ATPase in the colon mucosa was not affected. There was no damage of the epithelial cells as determined by lactic acid dehydrogenase release. These results indicate that neither inhibition of Na+,K(+)-ATPase nor damage of the colon epithelium are involved in the secretory effect of sennosides or rhein. The increased paracellular permeability of small molecules fits into the concept of stimulation of active chloride secretion by sennosides, which is electrochemically and osmotically balanced by an increase in Na+ and H2O flow via the paracellular pathway.

Animals↗
PubMed1994

Isolation of a human intestinal anaerobe, Bifidobacterium sp. strain SEN, capable of hydrolyzing sennosides to sennidins.

A strictly anaerobic bacterium capable of metabolizing sennosides was isolated from human feces and identified as Bifidobacterium sp., named strain SEN. The bacterium hydrolyzed sennosides A and B to sennidins A and B via sennidin A and B 8-monoglucosides, respectively. Among nine species of Bifidobacterium having beta-glucosidase activity, only Bifidobacterium dentium and B. adolescentis metabolized sennoside B to sennidin B, suggesting that the sennoside-metabolizing bacteria produce a novel type of beta-glucosidase capable of hydrolyzing sennosides to sennidins.

Anthracenes↗
PubMed1988

Effect of sennosides on colon motility in cats.

The actions of sennosides on colonic motility are incompletely understood. We therefore studied the effects of sennosides A + B on colonic myoelectric activity and transit of a radio-opaque meal in 7 conscious cats. Intraduodenal application of sennosides (2 mg/kg body weight) accelerated the half colon transit time from 60 +/- 10 (SEM) to 43 +/- 7 min. At the same time the ratio of long-spike bursts to short-spike bursts was changed from 0.22 to 10.1. Loperamide, an antidiarrheal agent, had the opposite effect. The overall spike activity was not altered by sennosides, but increased by loperamide. It is concluded that the propulsive action of sennosides in the colon is reflected by myoelectric patterns and not by the total number of spikes.

Animals↗
PubMed1993

Chronic sennoside treatment does not cause habituation and secondary hyperaldosteronism in rats.

Rats were treated with sennosides (6 x 10, 6 x 40 or 2 x 30 mg/kg weekly) or with danthron (6 x 500 mg/kg weekly) for 6 months. The laxative effect as measured by faecal wet weight during the first 10 h after treatment increased 3- to 4-fold by the higher sennoside doses (daily or intermittently) and 1- to 3-fold by danthron. The low sennoside dose had no measurable effect except on the 1st day (2 fold) compared with the control group. Mean faecal water content increased from 53% (controls) to 66-79% in rats treated with high sennoside doses and to 57 (1st day) -69% in danthron-treated rats. Serum aldosterone levels and mucosal Na(+)-K(+)-ATPase activities in the small intestine and colon did not change with treatment. There were no signs of habituation or secondary hyperaldosteronism due to sennosides or danthron in spite of chronic diarrhoea over 6 months.

Aldosterone↗
PubMed1998

The effect of sennosides on colonic mucosal histology and bowel preparation.

INTRODUCTION: A single high dose of sennosides is often used to optimize bowel preparation for diagnostic procedures. From previous studies it is suspected that sennosides in such a dose cause acute damage to the colonic mucosa. This study was designed to determine any effects of sennosides on histology of colonic mucosa and on bowel preparation. RESULTS: In a prospective study 171 patients were randomized for bowel preparation. 84 patients received 1 ml/kg (maximal 75 ml) of a syrup containing 2.0 mg/ml sennoside A and B and 3-5 l of a lavage solution (Sen), 87 patients only received 3-5 l lavage solution (NSen). All patients completed a questionnaire on which patient tolerance was scored. Another questionnaire was completed by the endoscopist, recording quality of the preparation. From the 40 patients with a normal colon (19 Sen, 21 NSen) a biopsy was taken from the sigmoid colon and analyzed for morphological abnormalities. No difference could be demonstrated in tolerance or quality of bowel preparation between the two groups. A marked increase of mononuclear infiltrate in the lamina propria was observed in Sen compared to NSen: in 10/19 vs. 2/21 patients respectively, p < 0.0005. CONCLUSION: As these microscopic effects could hamper the interpretation of colonic biopsies, bowel preparation without sennosides is to be recommended.

Adolescent↗