Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All cells, from bacterial to human, have a common, intricate response to stress that protects them from injury. Heat shock proteins (Hsps), also known as stress proteins and molecular chaperones, play a central role in protecting cellular homeostatic processes from environmental and physiologic insult by preserving the structure of normal proteins and repairing or removing damaged ones. An understanding of the interplay between Hsps and cell stress tolerance will provide new tools for treatment and drug design that maximise preservation or restoration of health. For example, the increased vulnerability of tissues to injury in some conditions, such as ageing, diabetes mellitus and menopause, or with the use of certain drugs,, such as some antihypertensive medications, is associated with an impaired Hsp response. Additionally, diseases that are associated with tissue oxidation, free radical formation, disorders of protein folding, or inflammation, may be improved therapeutically by elevated expression of Hsps. The accumulation of Hsps, whether induced physiologically, pharmacologically, genetically, or by direct administration of the proteins, is known to protect the organism from a great variety of pathological conditions, including myocardial infarction, stroke, sepsis, viral infection, trauma, neurodegenerative diseases, retinal damage, congestive heart failure, arthritis, sunburn, colitis, gastric ulcer, diabetic complications and transplanted organ failure. Conversely, lowering Hsps in cancer tissues can amplify the effectiveness of chemo- or radiotherapy. Treatments and agents that induce Hsps include hyperthermia, heavy metals (zinc and tin), salicylates, dexamethasone, cocaine, nicotine, alcohol, alpha-adrenergic agonists, PPAR-gamma agonists, bimoclomol, geldanamycin, geranylgeranylacetone and cyclopentenone prostanoids. Compounds that suppress Hsps include quercetin (a bioflavinoid), 15-deoxyspergualin (an immunosuppressive agent) and retinoic acid. Researchers who are cognisant of the Hsp-related effects of these and other agents will be able to use them to develop new therapeutic paradigms.
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PMID:Heat shock proteins: new keys to the development of cytoprotective therapies. 1599 80

Telmisartan is an angiotensin II T1 receptor blocker (ARB) with partial peroxisome proliferator-activated receptor gamma (PPARgamma) agonistic properties; two actions that are suggested to be efficacious for protecting against gastric ulcers. Hence, the aim of the present study was to evaluate the gastroprotective effect of telmisartan (1, 3, and 10 mg/kg) on indomethacin- and cold restraint stress (CRS)-induced gastric ulcer models in rats. Candesartan, another ARB with the lowest PPARgamma affinity, was used to justify the possible role of PPARgamma agonistic activity of telmisartan in gastroprotection. Ranitidine was used as a reference drug. Pre-treatment with telmisartan dose-dependently attenuated gastric ulcer indices induced by both models. The protective effect of telmisartan was accompanied by a significant rise in gastric mucosal nitric oxide (as nitrite/nitrate) with a concomitant fall in malondialdehyde concentrations as compared to the corresponding non-treated groups. Moreover, telmisartan significantly reduced free and total acid outputs in indomethacin-treated rats. On the other hand, telmisartan at the doses used did not alter gastric juice pH, peptic activity, mucin concentration or gastric mucosal prostaglandin E2 content in both ulcer models. The telmisartan-treated rats exhibited greater protection from gastric ulceration than candesartan-treated animals. In conclusion, telmisartan, in a dose-dependent manner, protected rats' gastric mucosa from ulcerations possibly through its anti-oxidant action against oxidative stress induced by either indomethacin or CRS. Also, the greater gastroprotection afforded by telmisartan compared to candesartan could be partly ascribed to its PPARgamma-inducing property.
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PMID:Gastroprotective effects of telmisartan on experimentally-induced gastric ulcers in rats. 1982 1

Garlic (Allium sativum, Liliaceae) is used widely as a spice and medicinal herb not only in its native region (Central Asia and northeastern Iran) but also all around the world. Garlic has abundance chemical compounds such as allicin, alliin, S-allyl cysteines, thiacremonone, diallyl-disulfide, diallylsulfide, and others. This medicinal plant and its constituents offer a lot of benefits including free-radical scavenging, anti-inflammatory, anticholesterolemic, anti-gastric ulcer, antimicrobial, anticancer, and antioxidant properties. Garlic also modulates the activity of several metabolizing enzymes. This review summarizes various in vitro and animal studies on the protective effects of garlic against natural and chemical toxicities. It has been shown that garlic and its major components can ameliorate the toxicity of different agents in brain, kidney, blood, liver, embryo, spleen, pancreas, heart, reproductive system in part through radical scavenging, antioxidant effect, reducing lipid peroxidation, anti-inflammatory, chelating agent, cytoprotective activities, increase protein synthesis in damaged tissues, suppressing apoptosis, modulation of p53, phosphoinositide 3-kinase, Akt, nuclear factor (erythroid-derived 2)-like 2, antioxidant responsive element, p38 MAPK, inducible nitric oxide synthase, cyclooxygenase-2, cytosolic phospholipases A2, cleaved-caspase-9, cleaved-caspase-3 Bcl-2, Bcl-2-associated X, peroxisome proliferator-activated receptor gamma, NF-jB, nuclear factor-kappaB signaling pathways and cytochrome P450 enzymes. With controlled clinical trials, garlic may be introduced as a universal antidote or protective plant against many toxic agents.
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PMID:Garlic (Allium sativum) as an antidote or a protective agent against natural or chemical toxicities: A comprehensive update review. 3206 26