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Curcumin mitigated ischemic and hyperhomocysteinemic cerebral microvascular mitochondrial mitophagy by decreasing oxidative and inflammatory stresses
Author(s) -
Kapoor Shray,
Tyagi Neetu,
Qipshidze Natia,
Givvimani Srikanth,
Kandel Madhavi,
Tyagi Suresh C
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.604.19
Subject(s) - oxidative stress , mitophagy , curcumin , inflammation , hyperhomocysteinemia , homocysteine , ischemia , endocrinology , superoxide dismutase , medicine , cystathionine beta synthase , chemistry , pharmacology , biochemistry , apoptosis , autophagy , enzyme , cysteine
Previous studies have shown that ischemia and hyperhomocysteinemia (HHcy) cause cerebral microvascular permeability; however, it was unclear whether the individuals with genetic HHcy were more prone to brain damage then the individuals with normal levels of homocysteine. Interestingly, curcumin mitigated the inflammation. Therefore we hypothesize that Hcy induced oxidative stress and inflammation after ischemia was ameliorated by Curcumin treatment. To test this hypothesis ischemia was created by inserting a wire in carotid artery in wild type (WT) and cystathionine beta synthase heterozygote knockout (CBS−/+) mice. The ischemic and sham mice were treated with and without curcumin (300 mg/kg) for 4 wks. The levels of mitochondrial mitophagy and oxidative stress were measured by oxidants (p47, p22, gp91phox) and anti‐oxidants (catalase, superoxide dismutase‐2, thioredoxin) by Western blot. The levels COX‐2, ICAM‐1 and PPARgamma were measured as inflammatory markers. The activity of NFkB was measured by EMSA. The results suggested that there was increase in p47, p22 in the ischemic and HHcy mice. Curcumin treatment mitigated mitochondrial mitophagy, in part, by increasing in NFkB activation. We concluded that Hcy caused oxidative stress and inflammation after ischemia. The treatment of curcumin ameliorated the mitophagy, oxidative stress and inflammation in both the ischemia and HHcy mice.