الفهرس 
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Abstract
Inflammation is defined as multifaceted non-specific host reaction that results from and accompanies the immune response in vivo. It is, by far, classified into acute and chronic that differs in their clinical, pathological and chronological course. The immediate and early response to injury is the acute form of inflammation, which lasts from few minutes up to few days. Its main characteristics are edema and recruitment of leukocytes.
The process of acute inflammation is controlled by diverse inflammatory regulators that include adhesion molecules as selectins and integrins, which are responsible for leukocytes adhesion to endothelial wall. Then, chemotaxis and recruitment of other leukocytes to site of inflammation are controlled by a diverse group of intracellular-signaling proteins, namely cytokines, among which is TNF-α, which possesses a variety of biological actions. Its prime importance in inflammation, besides the recruitment of neutrophils and monocytes is to activate these cells to eradicate microbes.
In view of such consideration, the design of the present work was set to study the impact of some drugs, in common use in ACS, on the course of an experimentally-induced acute inflammation in rats. The probed drugs were clopidogrel and low dose acetyl salicylic acid as antiplatelets, rosuvastatin as one of the statins and the anti-inflammatory indomethacin as control.
The present work was conducted on approximately 49 male albino rats of body weight ranging from 150-200 mg. Rats were divided into 2 major groups; control group and treated group, each group was subdivided into several subgroups of 7 rats each:
I. Control non-treated group:
Subgroup I: In this subgroup, the air pouches induced in the rats was injected with 2 ml saline instead of carrageenan, serving as control.
Subgroup II: The rats received 1ml of 1% gum acacia (the suspending agent of drugs) orally as control for six days starting from the day of induction of inflammation. This subgroup served to estimate reference values for the parameters studied.
II. Treated group:
After induction of acute inflammation in these rats by carrageenan air pouch model, they were divided into 5 subgroups (each of 7 rats) according to treatment with the studied drugs, namely:
Subgroup IIΙ: The rats received clopidogrel suspended in 1% gum acacia, in a dose of 30 mg/kg/day orally for six days starting from the day of induction of inflammation.
Subgroup IV: The rats received acetyl salicylic acid suspended in 1% gum acacia, in a dose of 30 mg/kg/day orally for six days starting from the day of induction of inflammation.
Subgroup V: The rats received rosuvastatin suspended in 1% gum acacia, in a dose of 20 mg/kg/day orally for six days starting from the day of induction of inflammation.
Subgroup VI: The rats received a combination of clopidogrel, acetyl salicylic acid and rosuvastatin in their respective doses suspended in 1% gum acacia, for six days starting from the day of induction of inflammation.
Subgroup VII: The rats received indomethacin suspended in 1% gum acacia, in a dose of 1 mg\kg\day orally for six days starting from the day of induction of inflammation.
Acute inflammation was induced by carrageenan air pouch model. On the first day 20 ml air was injected into the interscapular area of the back in the dorsum of the rats under complete sterile conditions. Two days later, another 10 ml of air was injected at the same site. On the fifth day after the first injection, a further 10 ml of air was injected into the pouch. Twenty-four hours later, carrageenan (2 ml of a 1% solution in sterile saline) was injected into the air pouch. All of the injections were performed after the rats had been anaesthetized with ether. Six hours after the carrageenan injection, the rats were anaesthetized with ether and the pouch was carefully opened by a small incision. The exudate was collected and transferred to a sterile tube. The following parameters were determine; non-immunological estimates, namely exudate volume, exudate total leukocytic cell count, exudate differential leukocytic cell counts, neutrophil adherence capacity according to the method described by (McGregor et al) and neutrophil phagocytosis according to the method described by (Stossel) and an immunological estimate namely TNF-α assay in exudate.