Gastrointestinal tract inhibition

Gastrointestinal tract Inhibition of most gut hormones, gastric acid, pepsin, bile and colonic fluid secretion... 

Prostaglandins whose synthesis involves COX-1 are largely responsible for maintenance and protection of the gastrointestinal tract (inhibiting acid production and stimulating mucous production), while prostaglandins whose synthesis involves COX-2 are responsible for inflammation and pain. 

GIF Peptide Gastrointestinal tract Inhibition of gastric secretion and... 

The primary sites and effects of drug-drug interactions involving other medications and MPA are likely to be decreased absorption in the gastrointestinal tract, inhibition of enterohepatic cycling, and inhibition of transport of the primary phenolic glucuronide metabolite. Meal consumption just before oral intake of MMF delays absorption, causing a reduction in the maximal concentration by about... 

The modes of action for niclosamide are interference with respiration and blockade of glucose uptake. It uncouples oxidative phosphorylation in both mammalian and taenioid mitochondria (22,23), inhibiting the anaerobic incorporation of inorganic phosphate into adenosine triphosphate (ATP). Tapeworms are very sensitive to niclosamide because they depend on the anaerobic metaboHsm of carbohydrates as their major source of energy. Niclosamide has selective toxicity for the parasites as compared with the host because Httle niclosamide is absorbed from the gastrointestinal tract. Adverse effects are uncommon, except for occasional gastrointestinal upset. 

The final mechanism of action of PTH involves the activation of vitamin D3 through the stimulation of la-hydroxylase in the kidney. In the gastrointestinal tract, vitamin D3 is essential for the absorption of calcium. Enhanced absorption of calcium from dietary sources serves to further increase the concentration of calcium in the blood. Many foods, in particular, dairy products, which are rich in calcium, are fortified with vitamin D. The release of PTH from the parathyroid glands is regulated by plasma calcium levels through negative feedback. A decrease in the level of calcium in the blood stimulates the secretion of PTH and an increase in the calcium level in the blood inhibits it. 

Niclosamide inhibits oxidative phosphorylation and stimulates adenosine tripho-sphatese activity in the mitochondria of cestodes, killing the scolex and proximal segments of the tapeworm both in vitro and in vivo. The scolex of the tapeworm, then loosened from the gut wall, may be digested in the intestine and thus may not be identified in the stool even after extensive purging [90,91], Niclosamide is not appreciably absorbed from the gastrointestinal tract [92,93] and the side effects have primarily been limited to gastrointestinal symptoms. 

Lanas A, Panes J, Pique JM Clinical implications of COX-1 and/or COX-2 inhibition for the distal gastrointestinal tract. Curr Pharm Des 2003 9 2253-2266. 

May cause severe and painful irritation of the eyes, nose, throat, and lungs. Severe exposure can cause accumulation of fluid in the lungs (pulmonary edema). Inhalation toxicity similar to HC1 and HF. May cause second or third degree burns upon short contact with skin surfaces. Oral ingestion may result in tissue destruction of the gastrointestinal tract. High overexposure may inhibit cholinesterase. 

The osteoprotegerin (OPG), also known as OCIF, TR1, or FDCR-1, is the first soluble protein that belongs to the TNF superfamily (Simonet et al. 1997 Kwon et al. 1998 Yun et al. 1998). Unlike RANK and RANKL, OPG is expressed in high concentrations in a variety of tissues and cellular types such as skin, bones, large arteries, and the gastrointestinal tract (Simonet et al. 1997). In bone, OPG is produced by stromal/OB cells (Hofbauer et al. 1999) and works as a decoy receptor for RANKL, competing with RANK for binding RANKL. Therefore, OPG is a potent inhibitor of the OCS. In vitro, OPG inhibits the differentiation and survival of osteoclast precursors, blocks their activation, and induces their apoptosis (Lacey et al. 1998 Yasuda et al. 1998 Hofbauer et al. 

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