080901 the Coxibs, Selective Inhibitors of Cyclooxygenase-2
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Taurine Prevents Ibuprofen-Induced Gastric Mucosal Lesions and Influences Endogenous Antioxidant Status of Stomach in Rats
Research Article TheScientificWorldJOURNAL (2004) 4, 1046–1054 ISSN 1537-744X; DOI 10.1100/tsw.2004.207 Taurine Prevents Ibuprofen-Induced Gastric Mucosal Lesions and Influences Endogenous Antioxidant Status of Stomach in Rats T. Balasubramanian1,*, M. Somasundaram1, and A. John William Felix2 1Department of Physiology, 2Department of Community Medicine, Rajah Muthiah Medical College, Annamalai University, Annamalainagar-608 002, Tamilnadu, India E-mails: [email protected], [email protected], [email protected] Received October 6, 2004; Revised November 25, 2004; Accepted November 29, 2004; Published December 6, 2004 Recently, free radical–induced tissue damage is implicated in the nonsteroidal anti- inflammatory drugs (NSAIDs)–involved gastric mucosal lesion. Administration of taurine, an endogenous antioxidant, is reported to be beneficial in various clinical conditions. Therefore, we decided to study the protective effect of taurine in ibuprofen-induced gastropathy and the effects of administration of taurine on the endogenous antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX), and reduced glutathione (GSH) of stomach. In rats, administration of taurine orally for three consecutive days (250 mg/kg body weight) protected the gastric mucosa from ibuprofen-induced, acute gastric mucosal lesion. In ibuprofen-treated rats, the lipid peroxidation measured as thiobarbituric acid reactive substances (TBARS), a marker for free radical–induced tissue damage, is also significantly decreased by taurine. Ibuprofen treatment resulted in a significant increase in the activities of total SOD, manganese SOD (Mn-SOD), and GPX and reduced GSH. Taurine administration in ibuprofen-treated rats also showed a significant increase in the activities of the antioxidant enzymes namely total SOD, Mn-SOD, GPX, CAT, and the level of reduced GSH. -
Effects of Intramuscular Diclofenac Use on Lipid
Sushma Sharma & Archana Thakur. Int. Res. J. Pharm. 2017, 8 (1) INTERNATIONAL RESEARCH JOURNAL OF PHARMACY www.irjponline.com ISSN 2230 – 8407 Research Article EFFECTS OF INTRAMUSCULAR DICLOFENAC USE ON LIPID PEROXIDATION AND SKELETAL MUSCLE HISTOLOGY IN BALB-C MICE Sushma Sharma and Archana Thakur * Department of Biosciences, Himachal Pradesh University, Summer Hill, Shimla, India *Corresponding Author Email: [email protected] Article Received on: 13/12/16 Revised on: 23/12/16 Approved for publication: 12/01/17 DOI: 10.7897/2230-8407.08014 ABSTRACT Diclofenac is a nonsteroidal anti-inflammatory drug that is widely used for the treatment of musculoskeletal complaints, osteoarthritis, rheumatoid arthritis, ankylosing spondylitis and acute muscle pain conditions. There is considerable interest in the toxicity of diclofenac because of its clinical uses. In the present study, the sub-chronic administration of diclofenac (10 mg/kg body weight; 30 days) resulted in various changes in activity of SOD enzyme (a marker of oxidative stress) and lipid peroxidation levels of mice. Changes in the activity of enzyme represent adaptive responses in muscle after diclofenac treatment. Results show that diclofenac is a strong inducer of oxidative stress. Increase in the formation of thiobarbituric acid reactive species (TBARS) and SOD activity is observed which indicates a link between oxidative stress and muscular toxicity. Maximum increase is seen in drug treated mice at 30 days’ stage of investigation. Key words: Diclofenac, SOD, lipid peroxidation INTRODUCTION Normal healthy looking mice showing no sign of morbidity were divided into following groups: Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the a) Mice in the first group (Group I) comprised of age matched most commonly prescribed categories of drugs worldwide in the control mice. -
Role of Active Oxygen, Lipid Peroxidation, and Antioxidants In
732 Gut 1993; 34: 732-737 Role of active oxygen, lipid peroxidation, and antioxidants in the pathogenesis of gastric mucosal Gut: first published as 10.1136/gut.34.6.732 on 1 June 1993. Downloaded from injury induced by indomethacin in rats T Yoshikawa, Y Naito, A Kishi, T Tomii, T Kaneko, S linuma, H Ichikawa, M Yasuda, S Takahashi, M Kondo Abstract role of reactive oxygen species in mediating the The roles of active oxygen, lipid peroxidation, microvascular disturbance that preceded gastric and the antioxidative defence mechanism in mucosal injury induced by several kinds of stress gastric mucosal injury induced by treatment and ischaemia-reperfusion." 12 Furthermore, with indomethacin in rats were investigated. lipid peroxidation mediated by oxygen free The total area of gastric erosions and concen- radicals is believed to be an important cause of tration of lipid peroxides in the gastric mucosa destruction and damage to cell membranes, increased with time after administration of because polyunsaturated fatty acids of the indomethacin (20 mg/kg, orally). The a- cellular membranes are degraded by the lipid tocopherol:total cholesterol ratio in serum was peroxidation with consequent disruption of significantly decreased and the activity of membrane integrity.'3 Membrane peroxidation glutathione peroxidase, an important enzyme can lead to changes in membrane fluidity and to scavenger of lipid peroxides, was inhibited permeability, enhanced rates ofprotein degrada- by the administration of indomethacin. Treat- tion, and ultimately, cell lysis. We have already ments with superoxide dismutase and catalase reported that lipid peroxidation plays a signifi- inhibited the increases in gastric mucosal cant part in the pathogenesis of gastric mucosal erosions and lipid peroxides in the gastric lesions induced by water immersion restraint mucosa, and the reduction of serum stress, burn shock, and ischemia-reperfusion.I'l6 a-tocopherol. -
Rofecoxib Versus Ibuprofen for Acute Treatment of Migraine: a Randomised Placebo Controlled Trial U K Misra, M Jose, J Kalita
720 Postgrad Med J: first published as 10.1136/pgmj.2003.017160 on 3 December 2004. Downloaded from ORIGINAL ARTICLE Rofecoxib versus ibuprofen for acute treatment of migraine: a randomised placebo controlled trial U K Misra, M Jose, J Kalita ............................................................................................................................... Postgrad Med J 2004;80:720–723. doi: 10.1136/pgmj.2003.012393 Background: Rofecoxib is a potent cyclo-oxygenase-2 inhibitor with a long duration of action. Its role in migraine has not been systematically evaluated. Aim: To study the efficacy of rofecoxib in migraine. Method: In a randomised placebo controlled trial rofecoxib 25 mg, ibuprofen 400 mg, and placebo were compared regarding their efficacy in relieving acute migraine attack. Migraine patients with 2–6 attacks per month were recruited. Headache severity, functional disability, and severity of associated symptoms were graded on a 0–3 scale. The primary endpoint was pain relief at two hours. Relief of associated symptoms and sustained pain relief for 24 hours were also noted. See end of article for Result: One hundred and twenty four patients were randomised into rofecoxib (42), ibuprofen (40), and authors’ affiliations placebo (42) groups. One hundred and one patients were followed up: 33 on rofecoxib, 35 ibuprofen, ....................... and 33 placebo. Patients’ ages ranged from 16–62 (mean 31.4) years, and 83 were females. Pain relief Correspondence to: at two hours was noted in 45.5% on rofecoxib, 55.6% on ibuprofen, and 9.1% in the placebo group. The Professor Usha Kant Misra, associated symptoms at two hours were reduced in 39.4% on rofecoxib, 50% on ibuprofen, and 9.1% in Department of Neurology, the placebo group. -
TOTAL JOINT SUPPORT (Formerly Glucosamine Plus)
TOTAL JOINT SUPPORT (Formerly Glucosamine Plus) Ingredients: Glucosamine Sulphate 100mg, N-Acetyl Glucosamine 50mg, L-Glutathione 2mg, N-Acetyl Cysteine 5mg, L-Cysteine 50mg, L-Glutamic Acid 50mg, L-Glycine 50mg, L-Taurine 25mg, Vitamin C 50mg, Vitamin E (Succinate) 25i.u, Pantothenic Acid 50mg, Soluble Trachea 25mg, Silymarin 5mg, Milk Thistle 100mg, Green Lipped Mussel 25mg. Supportive Function: Glucosamine Plus is a superb formula tested against individual nutrients for its synergistic action in supporting healthy bone and connective tissue. In the body, some glucosamine sulfate is converted to N-acetyl glucosamine (NAG), which is listed by the Merck Index in its own antiarthritic category. Liver detox, gastrointestinal and antioxidant nutrients all lend support that can be helpful when arthritis affects bone and connective tissue. Mucopolysaccharides are also important building blocks, which are furnished in this formula by green-lipped mussel. When is glucosamine support helpful? Osteoarthritis, tissue and joint pain, and injury. Clinical Applications/Research: Glucosamine Sulfate provides the essential building block needed for the construction and repair of joint cartilage, bone, tendons, and ligaments. Glucosamine further transforms into polyglycans that provide the foundation of synovial fluid and the lining of joints. Supplementation with glucosamine sulfate reduces pain and swelling and helps repair joints. Benefits become evident within 8 weeks. Continued supplementation is needed to maintain benefits (Drovanti A, et al, "Therapeutic activity of oral glucosamine sulfate in osteoarthritis: A placebo-controlled double blind investigation,"Clin Ther 1980: 3(4): 260-72). N-Acetyl Glucosamine (NAG) has been shown to reduce joint pain, swelling, and restricted motion in clinical trials. -
Studies on the Cardiovascular Effects of Selective COX-2 Inhibitors Show Mixed Results
Review: studies on the cardiovascular effects of Evid Based Med: first published as 10.1136/ebm.7.2.49 on 1 March 2002. Downloaded from selective COX-2 inhibitors show mixed results Mukherjee D, Nissen SE, Topol EJ. Risk of cardiovascular events associated with selective COX-2 inhibitors. JAMA 2001 Aug 22/29;286:954–9. QUESTION: In patients with arthritis, do rofecoxib or celecoxib increase the risk for cardiovascular events? Data sources increase 138%, 95% CI 39 to 300; number needed to Studies were identified by searching Medline (1998 to harm 146, CI 69 to 517}*. The Celecoxib Long-term February 2001) and the internet. The Adverse Events Arthritis Safety Study (CLASS) compared celecoxib 400 Reporting System was searched for US events on Octo- mg twice daily; ibuprofen 800 mg 3 times daily; and ber 12, 2000. diclofenac 75 mg twice daily, in 8059 patients with osteoarthritis or rheumatoid arthritis. Patients were Study selection allowed to take aspirin ( < 325 mg/day). Celecoxib and English language studies were selected if they were ran- non-steroidal anti-inflammatory drugs did not differ for domised, double blind, controlled trials reporting the cardiovascular event rates. 2 studies compared rofecoxib cardiovascular effects of celecoxib or rofecoxib. 12.5 mg/day; nabumetone 1000 mg/day; and placebo for 6 weeks in 1042 and 978 patients with osteoarthritis Data extraction of the knee. Patients were allowed to take low dose aspi- Data were extracted on study methods, patient charac- rin. In both studies, the groups did not differ for cardio- teristics, drug regimens, aspirin use, and cardiovascular vascular event rates. -
Cinnamon Aqueous Extract Attenuates Diclofenac Sodium And
veterinary sciences Article Cinnamon Aqueous Extract Attenuates Diclofenac Sodium and Oxytetracycline Mediated Hepato-Renal Toxicity and Modulates Oxidative Stress, Cell Apoptosis, and Inflammation in Male Albino Rats Gehad E. Elshopakey 1,* and Sara T. Elazab 2 1 Department of Clinical Pathology, Faculty of Veterinary Medicine, Mansoura University, Mansoura 35516, Egypt 2 Department of Pharmacology, Faculty of Veterinary Medicine, Mansoura University, Mansoura 35516, Egypt; [email protected] or [email protected] * Correspondence: [email protected] or [email protected]; Tel.: +20-102-392-3945 Abstract: Among commonly consumed anti-inflammatory and antimicrobial drugs are diclofenac sodium (DFS) and oxytetracycline (OTC), especially in developing countries because they are highly effective and cheap. However, the concomitant administration of anti-inflammatory drugs with antibiotics may exaggerate massive toxic effects on many organs. Cinnamon (Cinnamomum zeylanicum, Cin) is considered one of the most broadly utilized plants with various antioxidant and anti- inflammatory actions. This study aimed to evaluate the possible protective effects of cinnamon aqueous extract (Cin) against DFS and OTC hepato-renal toxicity. Eight groups (8/group) of adult male albino rats were treated orally for 15 days with physiological saline (control), Cin aqueous extract (300 mg/kg b.w.), OTC (200 mg/kg b.w.), single dose of DFS at the 14th day (100 mg/kg b.w.), DFS + OTC, Cin + DFS, Cin + OTC, and Cin + DFS + OTC. The administration of DFS and/or Citation: Elshopakey, G.E.; Elazab, S.T. Cinnamon Aqueous OTC significantly increased (p < 0.05) the serum levels of alanine aminotransferase, aspartate amino- Extract Attenuates Diclofenac transferase, alkaline phosphatase, urea, creatinine, and uric acid. -
Superoxide Dismutase) Antioxidant
PRODUCT DATA DOUGLAS LABORATORIES® 04/2012 1 S.O.D. (Superoxide Dismutase) Antioxidant DESCRIPTION S.O.D. (Superoxide Dismutase) from Douglas Laboratories contains 2,000 M.F. units of superoxide dismutase from porcine liver extract. FUNCTIONS Body cells and tissues are threatened continuously by damage caused by toxic free radicals and reactive oxygen species (e.g., peroxides) which are produced during normal oxygen metabolism, by other chemical reactions, and by toxic agents in the environment. Free radicals, once formed, are capable of disrupting metabolic activity and cell structure. When this occurs, additional free radicals are produced which, in turn, can result in more extensive damage to cells and tissues, particularly the oxidation of DNA, proteins, and membrane lipids. The uncontrolled production of free radicals is thought to be a major contributing factor to many degenerative pathologies. Superoxide dismutase (SOD) is a prime antioxidant enzyme found in two forms. One, complexed with zinc and copper, is localized in the cytosol, while the other, bound with manganese, is found in the mitochondrial matrix. Both forms of this metalloenzyme catalyze the inactivation of destructive reactive oxygen species by converting them to hydrogen peroxide which is then transformed to water and oxygen by the enzyme catalase. Superoxide dismutase has been shown to be useful in joint, gastrointestinal and respiratory health. INDICATIONS S.O.D. (Superoxide Dismutase) from Douglas Laboratories is a dietary adjunct for those who wish to supplement their diet with antioxidant enzymes. FORMULA (#7987) Each Capsule Contains: Superoxide Dismutase ...................... 2,000 M.F.units (from porcine liver extract) with naturally occurring catalase enzyme SUGGESTED USE Adults take 1 or more capsules daily or as directed by a healthcare professional. -
Nonsteroidal Antiinflammatory Drugs Inhibiting Prostanoid Efflux: As Easy As ABC?
Nonsteroidal antiinflammatory drugs inhibiting prostanoid efflux: As easy as ABC? Timothy D. Warner*† and Jane A. Mitchell‡ *The William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, United Kingdom; and ‡National Heart and Lung Institute, Imperial College School of Medicine, Dovehouse Street, London SW3 6LY, United Kingdom onsteroidal antiinflammatory may explain its antinociceptive proper- resistance proteins (MRP) form a sub- drugs (NSAIDs) and prosta- ties (7). Others have found therapeutic family within the ABC transporters. noids continue to be fascinat- effects of NSAID metabolites that are MRP1 is a high-affinity leukotriene C4 N ing research targets. Humans inactive on COX; sulindac sulfone is a transporter, and mice that harbor dele- have been using NSAIDs in one form or clear example. The NSAID sulindac is tions of this gene have an altered re- another, from folk remedies through to an inactive drug metabolized to a phar- sponse to inflammatory stimuli but are the products of modern pharmaceutical macologically active sulfide derivative, otherwise healthy and fertile. MRP2 is research, for thousands of years. How- which potently inhibits COX. Sulindac is the major transporter responsible for ever, we still have not characterized all also metabolized to a sulfone derivative the secretion of bilirubin glucuronides of the systems through which these that is inactive against COX. However, into bile (11). MRP1 and -4 may also be drugs produce their beneficial and like sulindac sulfide, sulindac sulfone involved in the transport of dehydroepi- harmful effects (1, 2). We are certain, both promotes cellular apoptosis and androsterone 3-sulfate (the most abun- from seminal work carried out in the dant circulating steroid in humans), and 1960s and early 1970s, that NSAIDs MRP4 transports conjugated steroids have the common property of inhibiting Some NSAIDs and bile acids (12). -
Side Effects of Dexibuprofen Have Been Ameliorated with Vitamin E Gamal El-Din A.M
BENHA VETERINARY MEDICAL JOURNAL, VOL. 36, NO. 1:382-392, March, 2019 Side effects of dexibuprofen have been ameliorated with vitamin E Gamal El-Din A.M. Shams, Suhair A. Abd El-Latif, Haydi H. El Din Abdallah Pharmacology Department, Faculty of Veterinary Medicine, Zagazig University, Egypt A B S T R A C T The present study was designed to define the effects of daily administration of 100 mg vitamin E\kg on side effects in mice treated with dexibuprofen (7.2 mg/kg, P.O once daily) for 21 consecutive days and its antioxidant scavenging capacity. Blood samples were collected from mice on 1st, 2nd, 14th, 21st days post –treatment and tissue samples were collected on 7th, 14th days post- treatment to assess the protective effects of vitamin E. The results indicated significant increase in antioxidant enzymes Glutathione peroxidase, dismutase superoxide dismutase(SOD)&catalase (CAT) together decrease the level of malondialdehyde besides diminished and in portal fibrosis and decrease in congestion of hepatic blood vessels and sinusoids caused by dexibuprofen administration as demonstrated by kidney histopathology Therefore, Vitamin E should be taken with dexibuprofen to decrease its side effects. Key words Antioxidant activity, Dexibuprofen, Histopathology, Vitamin E. ) BVMJ-36(1): 382-392, 2019) 1. INTRODUCTION (http://www.bvmj.bu.edu.eg Dexibuprofen is non-steroidal anti- between the two drugs was in the degree of inflammatory drug. It's the active recovery of platelet function. The effect of dextrorotatory enantiomer of ibuprofen. Most aspirin persisted for 24 h after the last dose ibuprofen formulations contain a racemic (remaining inhibition 50% respect to the mixture of both isomers (Hardikar, 2008). -
Clinical Outcomes of Aspirin Interaction with Other Non-Steroidal Anti- Inflammatory Drugs: a Systematic Review
J Pharm Pharm Sci (www.cspsCanada.org) 21, 48s – 73s, 2018 Clinical Outcomes of Aspirin Interaction with Other Non-Steroidal Anti- Inflammatory Drugs: A Systematic Review Zuhair Alqahtani and Fakhreddin Jamali Faculty of Pharmacy and Pharmaceutical Science, University of Alberta, Edmonton, Alberta, Canada. Received, March 16, 2018; Revised, March 30, 2018; Accepted, April 25, 2018; Published, April 27, 2018. ABSTRACT - Purpose: Concomitant use of some non-Aspirin nonsteroidal anti-inflammatory drugs (NANSAIDs) reduces the extent of platelet aggregation of Aspirin (acetylsalicylic acid). This is while many observational studies and clinical trials suggest that Aspirin reduces cardiovascular (CV) risk attributed to the use of NANSAIDs. Thus, the therapeutic outcome of the interaction needs to be assessed. Methods: We searched various databases up to October 2017 for molecular interaction studies between the drugs and long-term clinical outcomes based on randomized clinical trials and epidemiological observations that reported the effect estimates of CV risks (OR, RR or HR; 95% CI) of the interacting drugs alone or in combinations. Comparisons were made between outcomes after Aspirin alone, NANSAIDs alone and Aspirin with naproxen, ibuprofen, celecoxib, meloxicam, diclofenac or rofecoxib. Results: In total, 32 eligible studies (20 molecular interactions studies and 12 observational trials) were found. Conflicting in vitro/in vivo/ex vivo platelet aggregation data were found for ibuprofen, naproxen and celecoxib. Nevertheless, for naproxen, the interaction at the aggregation level did not amount to a loss of cardioprotective effects of Aspirin. Similarly, for ibuprofen, the results overwhelmingly suggest no negative clinical CV outcomes following the combination therapy. Meloxicam and rofecoxib neither interacted with Aspirin at the level of platelet aggregation nor altered clinical outcomes. -
VIOXX® (Rofecoxib Tablets and Oral Suspension)
VIOXX® (rofecoxib tablets and oral suspension) WARNING: RISK OF SERIOUS CARDIOVASCULAR AND GASTROINTESTINAL EVENTS Cardiovascular Thrombotic Events Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use (see WARNINGS). VIOXX is contraindicated in the setting of coronary artery bypass graft (CABG) surgery (see CONTRAINDICATIONS, WARNINGS). Gastrointestinal Bleeding, Ulceration, and Perforation NSAIDs cause an increased risk of serious gastrointestinal (GI) adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients and patients with a prior history of peptic ulcer disease and/or GI bleeding are at greater risk for serious GI events. (see WARNINGS). DESCRIPTION VIOXX® (rofecoxib) is a nonsteroidal anti-inflammatory drug (NSAID). The chemical name is 4-[4 (methylsulfonyl)phenyl]-3-phenyl-2(5H)-furanone. The molecular weight is 314.36. The empirical formula for rofecoxib is C17H14O4S, and it has the following chemical structure: O O O S H C 3 O Rofecoxib is a white to off-white to light yellow powder. It is sparingly soluble in acetone, slightly soluble in methanol and isopropyl acetate, very slightly soluble in ethanol, practically insoluble in octanol, and insoluble in water. Each tablet of VIOXX for oral administration contains either 12.5 mg, 25 mg, or 50 mg of rofecoxib and the following inactive ingredients: croscarmellose sodium, hydroxypropyl cellulose, lactose, magnesium stearate, microcrystalline cellulose, and yellow ferric oxide.