Premium
CURCUMIN PRE‐EXPOSURE IN VIVO PREVENTS ACETAMINOPHEN‐INDUCED APOPTOTIC AND NECROTIC CELL DEATHS IN THE LIVER
Author(s) -
Bulku Ellida,
Zinkovsky Daniel,
Patel Nirav,
Ray Sidhartha D.
Publication year - 2006
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.20.5.a1144-a
Subject(s) - curcumin , acetaminophen , pharmacology , in vivo , apoptosis , lipid peroxidation , curcuma , liver injury , oxidative stress , medicine , nephrotoxicity , programmed cell death , curcuminoid , toxicity , chemistry , traditional medicine , biology , biochemistry , microbiology and biotechnology
Curcumin (CUR; diferuloylmethane), a rhizome extract of Curcuma longa is commonly used as a food coloring and flavoring agent. Although Oriental and the Ayurvedic medicines have traditionally used CUR in the treatment of diseases, conventional medicine has just begun to recognize its potential therapeutic value. Numerous experiments conducted by researchers around the globe have demonstrated CUR's ability to halt or prevent certain types of cancer, stop inflammation, and improve cardiovascular health. However, very few studies have examined its ability to protect against drug‐induced organ injury. This study explored whether CUR pre‐exposure has the potential to prevent acetaminophen (AP)‐induced: (i) organ injuries (both hepatotoxicity and nephrotoxicity), in addition to (ii) apoptotic and necrotic cell deaths in the liver in vivo. Additional goals were to determine whether these events were linked to AP‐induced oxidative stress, bcl‐XL expression and the modes of cell death in the liver. In order to study CUR‐AP interaction, male B6C3F1 mice were gavaged with CUR (17 mg/kg, p.o.) for 12 days followed by a single AP exposure(400 mg/kg, ip). Four groups of animals (Control, CUR, APAP, CUR+AP) were sacrificed 24h after AP exposure. Results indicated that AP‐induced liver injury associated events, such as (ALT U/L:12 fold), lipid peroxidation (373%) and DNA fragmentation (325%) were considerably reduced to 3‐fold, 89% and 104% respectively in CUR+AP group. AP‐induced decrease in bcl‐XL expression was also alleviated by CUR exposure and this change was mirrored in the pattern of apoptotic and necrotic cell deaths. It appears that CUR may impart global organoprotection against drug‐induced organ toxicity by opposing events associated with both apoptosis and necrosis.