Pharmacology. 1988;36 Suppl 1:85-91.
Prostaglandin-mediated action of sennosides.
Beubler E, Kollar G.
Department of Experimental and Clinical Pharmacology, University of Graz, Austria.
The aim of this study was to investigate whether prostaglandins (PG) are involved in the mediation of sennoside-induced colonic fluid and electrolyte secretion. Oral administration of senna pod extract dose-dependently reversed net absorption of water, sodium and chloride to net secretion, increased potassium secretion and stimulated the release of PGE2 into the colonic lumen. Inhibition of PG biosynthesis by pretreatment of the rats with indomethacin significantly inhibited the effects of senna pod extract both on net fluid transport and on PGE2 release. The inhibitory effect of indomethacin on net fluid transport induced by senna pod extract was dose-dependent. It is concluded that sennosides exert their laxative action at least partially via stimulation of colonic fluid and electrolyte secretion, and that this secretion is mediated by stimulation of endogenous PGE2 formation.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3163424&dopt=Abstract constipation laxative
J Adolesc Health Care. 1988 Sep;9(5):394-7.
Weight control methods in high school wrestlers.
Woods ER, Wilson CD, Masland RP Jr.
Department of Pediatrics, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
Severe weight control methods used by high school wrestlers have caused concern about these students' growth and athletic performance. There are minimal prevalence data on a few methods of weight control used by wrestlers and no information on the relationship to body fat measurements. Weight control methods and the percent body fat of wrestlers (n = 49) were compared to competitive squash players (n = 20) and noncompetitive jogging and fitness students (n = 38) at an independent secondary school. Wrestlers used dieting (p = 0.0002), binging (p = 0.026, vomiting (p = 0.046), sweating (p = 0.0001), and fluid restriction to less than 2 cups/day (p = 0.0014) significantly more often than controls (squash players and jogging/fitness students). There was no difference between the wrestlers' and controls' use of fasting (p = 0.5) or exercising (p = 0.1). Neither group reported using a diuretic or laxative during the sports seasons. Although the wrestlers' percent body fat was lower than controls (mean for wrestlers = 10.3 +/- 3.5%, mean for controls = 12.4 +/- 3.7%, p = 0.01), wrestlers perceived their mean ideal weight to be less than their present weight (wrestlers = -1.56 +/- 6.20 lb, controls = +1.92 +/- 9.49 lb, p = 0.03). The methods of weight control practiced could potentially impair an adolescent's growth and development as well as increase the risk of dehydration or electrolyte imbalance during competition.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3170306&dopt=Abstract constipation laxative
Drug Metab Dispos. 2001 Sep;29(9):1229-35.
Induction of cytochromes P450 1A1 and 1B1 by emodin in human lung adenocarcinoma cell line CL5.
Wang HW, Chen TL, Yang PC, Ueng TH.
Institute of Toxicology, College of Medicine, National Taiwan University, 1 Jen Ai Road, Section 1, Taipei, Taiwan, Republic of China.
Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) is an active compound of many laxative herbal drugs. The present study aimed to determine the effects of emodin on cytochrome P450 (P450)-dependent monooxygenases of human lung adenocarcinoma CL5 cells. Treatment of CL5 cells with 100 microM emodin for 24 h induced benzo[a]pyrene hydroxylation, 7-ethoxyresorufin O-deethylation, and 7-ethoxycoumarin O-deethylation activities of S9 fractions. Immunoblot analysis of CL5 S9 proteins revealed that emodin induced proteins immunorelated to P450s 1A1 and 1B1. Northern blot analysis of total cellular RNA showed that emodin induced P450s 1A1 and 1B1 mRNA levels in CL5 cells. These inductive effects on P450 monooxygenase activity, protein, and mRNA were concentration- and time-dependent. Addition of emodin to CL5 cell microM S9 inhibited its 7-ethoxycoumarin O-deethylation activity. Treatment of CL5 cells with 10 microM 3-methylcholanthrene for 24 h induced monooxygenase activity and P450s 1A1 and 1B1 proteins and mRNA levels. Treatment of the lung cells with 100 microM emodin or purpurin (1,2,4-trihydroxyanthraquinone) for 24 h produced greater induction of P450s 1A1 and 1B1 mRNA than did anthraflavic acid (2,6-dihydroxyanthraquinone) or anthraquinone. The emodin treatment induced P450s 1A1 and 1B1 mRNA in human lung carcinoma NCI-H322 and breast cancer MCF-7 cells. Emodin induced P450 1A1, but not 1B1, mRNA in human hepatoma HepG2 cells. The present study demonstrates that emodin is an inducer of P450s 1A1 and 1B1 protein and mRNA in human lung adenocarcinoma CL5 cells. Modulation of P450 by emodin may be an important factor affecting metabolism and toxicity of the hydroxyanthraquinone in humans.
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