Effect of anti-inflammatory drugs on lysosomes and lysosomal enzymes from rat liver

Smith, Robert J.; Sabin, C; Gilchrest, Helen; Williams, Shirley

doi:10.1016/0006-2952(76)90129-5

Cited by 62 publications

(11 citation statements)

References 38 publications

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“…In this regard, ibuprofen could protect the ischemic myocardium by: (a) inhibition of prostaglandin synthesis (3,26); (b) inhibition of platelet aggregation (21,36); (c) activation of endo genous corticosteroid secretion (24); (d) prevention of cardiac arrhythmias; (e) reduction of myocardial oxygen demand (35), or (0 membrane stabilization (15,19,28).…”

Section: Discussionmentioning

confidence: 99%

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Beneficial Effects of Ibuprofen in Acute Myocardial Ischemia

Lefer

Polansky²

1979

Cardiology

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Ibuprofen, a nonsteroidal anti-inflammatory agent, was studied in the early stages of myocardial ischemia in order to determine whether it helps preserve myocardial integrity. Ibuprofen was administered intravenously at a dose of 12.5 mg/kg at the time of coronary artery occlusion and again 2.5 h later. Ibuprofen significantly prevented the loss of myocardial creatine phosphokinase (CPK) release in ischemic cardiac tissue. In addition, this drug significantly returned S-T segment elevation toward normal values, and significantly prevented the myocardial loss of compounds having free amino nitrogen groups, an index of proteolysis. Although ibuprofen moderated the increased plasma CPK activity, plasma CPK values 5 h after coronary occlusion were above control values. Thus, ibuprofen significantly prevented alterations in three of the four indices used to assess myocardial ischemic damage. The protective mechanism of ibuprofen may be via stabilization of cellular membranes (i.e., lysosomal membranes) and to a lesser extent on reduction in myocardial oxygen demand.

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Section: Discussionmentioning

confidence: 99%

“…Ibuprofen is a nonsteroidal anti-inflammatory agent that inhibits prosta glandin release and stabilizes lysosomal membranes (15,19,28) without exerting a pressor effect (7). Earlier, Mclean et al (17) found ibuprofen to protect the ischemic rat myocardium against subsequent infarct formation, several days later.…”

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confidence: 99%

Beneficial Effects of Ibuprofen in Acute Myocardial Ischemia

Lefer

Polansky²

1979

Cardiology

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“…To study the membrane-stabilizing property of anti-inflammatory agents, erythrocytes have been used as a model. There are several reports to show a similar order o f potencies for anti-inflammatory effects and stabiliza tion of lysosomal [7] and erythrocyte [3,5] thiosemicarbazone] indoles resulted in an in creased ability o f these compounds to protect erythrocytes against hypo-osmotic hemoly sis. Introduction of an amino group at position 3 of the aryl group attached to the indole moiety of methyl-substituted thiosemicarba zone indoles (compounds V III and IX) caused potentiation o f the membrane-stabil izing effect.…”

Section: Resultsmentioning

confidence: 85%

Membrane Stabilization and Inhibition of Lipid Peroxidation by Anti-Inflammatory Indoles

Kaur¹,

Ali²

1982

Pharmacology

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Nine 2-aryl-3-[4-(substituted phenyl)-3-thiosemicarbazone] indoles were evaluated for their ability to protect the human erythrocyte membrane against hypo-osmotic hemolysis and inhibit lipid peroxidation in rat liver homogenate in vitro. All compounds caused membrane stabilization and inhibition of lipid peroxidation when tested at final concentrations of 5 × 10^–4 and 2.5 × 10^–5 mol/l, respectively. These biochemical effects were not related to the anti-inflammatory property exhibited by the compounds.

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“…Ibuprofen is also an effective membranestabilizing agent, including stabilization of lysosomal membranes [11,21], Although this subcellular effect o f ibuprofen is superior to that o f many other anti-inflammatory agents, and may be very important in pre venting mortality in circulatory shock [23] and in preventing the extension o f ischemic damage in myocardial ischemia [9,11,16], it is probably o f no great significance in arachidonate-induced sudden death, since this phe nomenon occurs so rapidly (i.e.. 3-5 min).…”

Section: Resultsmentioning

confidence: 99%

Protective Actions of Ibuprofen in Arachidonate-Induced Sudden Death

Roth¹,

Burke²,

Lefer³

1983

Pharmacology

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Sodium arachidonate given intravenously at a dose of 2 mg/kg is uniformly lethal in rabbits. Rabbits die within 2–5 min following a dramatic decrease in mean arterial blood pressure (MABP), and in circulating platelets, and a large increase in plasma thromboxane B₂(TXB₂) concentration. The nonsteroidal anti-inflammatory agent, ibuprofen, given 15 min prior to challenge with sodium arachidonate, significantly protects against the abrupt decrease in MABP and in circulating platelets and prevents the increase in circulating TxB₂ concentrations. These rabbits all survive the lethal efects of arachidonic acid when given ibuprofen at doses of 0.75, 6.25 or 12.5 mg/kg intravenously 15 min prior to arachidonate challenge. At 0.375 mg/kg, only 20% of the animals survive. Concomitant with survival is a significant attenuation of the decrease in MABP (84 ± 8 mm Hg without ibuprofen vs. 1 ± 1 to 33 ± 12 mm Hg with 12.5–0.75 mg/kg ibuprofen). Similarly, these rabbits show a greatly reduced loss of circulating platelets, and virtually no increases in the formation of TxB₂. Ibuprofen protects against arachidonate-induced sudden death in a dose-related manner. The mechanism of the protection appears to involve prevention of adherence or aggregation of platelets and the subsequent formation of thromboxane A₂. The net result is prevention of pulmonary thrombosis, the major pathological event in triggering sudden death.

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Effect of anti-inflammatory drugs on lysosomes and lysosomal enzymes from rat liver

Cited by 62 publications

References 38 publications

Beneficial Effects of Ibuprofen in Acute Myocardial Ischemia

Beneficial Effects of Ibuprofen in Acute Myocardial Ischemia

Membrane Stabilization and Inhibition of Lipid Peroxidation by Anti-Inflammatory Indoles

Protective Actions of Ibuprofen in Arachidonate-Induced Sudden Death

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