@article{MAKHILLRJBS202116111530,
    title = {Tenofovir/Lamivudine/Efavirenz-Induced Hepatotoxicity: Cucurmin as a Potential Protective
Agent},
    journal = {Research Journal of Biological Sciences},
    volume = {16},
    number = {1},
    pages = {1-8},
    year = {2021},
    issn = {1815-8846},
    doi = {rjbsci.2021.1.8},
    url = {https://makhillpublications.co/view-article.php?issn=1815-8846&doi=rjbsci.2021.1.8},
    author = {Elias,Ruth and},
    keywords = {Antiretroviral,liver,toxicity,curcumin,protection,rat},
    abstract = {Tenofovir/Lamivudine/Efavirenz (TLE) is a
first-line agent used for the treatment of human
immunodeficiency virus (HIV). Its use has decreased HIV
progression, but the occurrence of hepatotoxicity is a
serious burden. Curcumin (CUM) is a polyphenol
compound which has potential therapeutic health benefits.
This study assessed its protective effect against
TLE-induced hepatotoxicity in Wistar rats. Forty adult
male Wistar rats (180-200 g) grouped into 8 of n = 5 were
used. Group I (Control) was orally administered with
normal saline (0.2 mL) daily. Groups II-IV were orally
administered with CUM (50, 100 and 200 mg kg<sup>&#150;1</sup>) daily.
Group V was orally administered with TLE
(300/300/600) mg kg<sup>&#150;1</sup>. Groups V1-VIII; were orally
administered with CUM (50, 100 and 200 mg kg<sup>&#150;1</sup>)
before the administration of TLE (300/300/600) mg kg<sup>&#150;1</sup>
daily. The rats were treated for 30 days. After treatment,
the rats were anesthetized and blood samples were
collected and assessed for serum liver function markers.
Liver samples were excised and assessed for oxidative
stress markers and histology. Serum aminotransferases,
bilirubin, lactate dehydrogenase alkaline phosphase,
gamma-glutamyl transferase, liver malondialdehyde
levels and liver weight were significantly (p<0.001)
increased in TLE administered rats when compared to
control. Body weight, liver catalase, glutathione (GSH),
superoxide dismutase and GSH peroxidase levels were
significantly (p<0.001) decreased in TLE-treated rats
when compared to control. TLE caused hepatocytes
necrosis. Interestingly, CUM supplementation abrogate
TLE-induced hepatotoxicity at 50 mg kg<sup>&#150;1</sup> (p<0.05),
100 mg kg<sup>&#150;1</sup> (p<0.01) and 200 mg kg<sup>&#150;1</sup> (p<0.001) when
compared to TLE. CUM may clinically prevent TLE
related hepatotoxicity.}
    }