Abstract
Carrageenan produces both inflammation and pain when injected in mouse paws via enhancement of reactive oxygen species formation. We have investigated an effect of astaxanthin extracted from Litopenaeus vannamei in carrageenan-induced mice paw edema and pain. The current study demonstrates interesting effects from astaxanthin treatment in mice: an inhibition of paw edema induced in hind paw, an increase in mechanical paw withdrawal threshold and thermal paw withdrawal latency, and a reduction in the amount of myeloperoxidase enzyme and lipid peroxidation products in the paw. Furthermore the effect was comparable to indomethacin, a standard treatment for inflammation symptoms. Due to adverse effects of indomethacin on cardiovascular and gastrointestinal systems, our study suggests promising prospect of astaxanthin extract as an anti-inflammatory alternative against carrageenan-induced paw edema and pain behavior.
Highlights
Inflammation is a cellular response to a traumatic injury, irritation from toxic chemicals, or infection caused by microbial pathogens
A significant increase in paw thickness was observed in all groups, the mice that received indomethacin or astaxanthin displayed significantly less edema
(100–150 mg/kg) and indomethacin-treated animals was observed. These results indicate that that astaxanthin was as effective as indomethacin in reducing inflammation-induced thermal and astaxanthin was as effective as indomethacin in reducing inflammation-induced thermal and mechanical hyperalgesia
Summary
Inflammation is a cellular response to a traumatic injury, irritation from toxic chemicals, or infection caused by microbial pathogens. This complex process involves numerous pathways of cellular and plasma origin with interrelated biological events, often leading to painful conditions, such as in rheumatoid arthritis, asthma, allergy, inflammatory bowel syndrome, atherosclerosis, and neurodegenerative disease [1,2]. Peroxynitrite (ONOO ) by combining with superoxide anion radicals, harmful to functional normal tissues [5,6]. This aforementioned statement reflects the role of reactive oxygen and nitrogen species in the pathophysiology of inflammation.
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