الفهرس 
TitleOnly 14 pages are availabe for public view
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Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common form of liver disease worldwide. NAFLD is defined as evidence of hepatic steatosis, revealed either by biopsy or imaging techniques, in the absence of substantial alcohol intake, viral hepatitis, steatogenic medications or congenital metabolic disorders. NAFLD is an increasingly recognized cause of liver-related morbidity and mortality NAFLD is commonly associated with obesity, type 2 diabetes mellitus, dyslipidemia and hypertension; NAFLD has also been regarded as a hepatic manifestation of metabolic syndrome.
No therapeutic treatments have proven effective for the treatment of NAFLD, and the treatment of NAFLD predominantly lies in lifestyle management. Other methods currently in use include weight loss drugs, physical activity, oral antidiabetic medication.
Propolis (honey bee glue) has been used as a popular folk medicine for its antibacterial, anti-inflammatory, antioxidative, immunostimulatory and carcinostatic properties.
The aim of this study was to evaluate the possible therapeutic effect of propolis ethanolic extract (PEE) on the experimental rat model of non- alcoholic fatty liver disease through modulation of hepatic expression of miR-34a and lipogenic transcription factors; SREBP-1c, ATF3, PPAR-α and SIRT1.
The study was conducted on 50 male Wistar rats (150-170 g) three months old. NAFLD model was induced in rats using high fat diet (HFD) that was given orally daily for 10 weeks. After the induction period, fatty liver was confirmed by ultrasound in the Diagnostic radiation department. The animals was separated into two groups; group I (Control group): consisted of 10 healthy male rats that was orally given normal diet. group II (NAFLD group): consisted of 40 NAFLD rats that subdivided into four subgroups: group IIA: consisted of 10 untreated NAFLD rats. group IIB: consisted of 10 NAFLD rats that was orally given 100mg/kg b.wt /day of propolis ethanolic extract (PEE) dissolved in dimethyl sulfoxide (DMSO) for four weeks. group IIC: consisted of 10 NAFLD rats that was orally given 200mg/kg b.wt /day of propolis ethanolic extract (PEE) dissolved in dimethyl sulfoxide (DMSO) for four weeks. group IID: consisted of 10 NAFLD rats that was orally given 300mg/kg b.wt /day of propolis ethanolic extract (PEE) dissolved in dimethyl sulfoxide (DMSO) for 4 weeks.
Summary & Conclusions
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After the treatment, animals was scarified by cervical dislocation and the liver was dissected then divided into three parts. The first part of liver tissue were excised for the determination of hepatic nuclear factor-κappa B (NF-κB) and the second part used for total RNA isolation for the determination of hepatic expression of Micro-RNA-34a (miR-34a), sterol regulatory element binding protein-1c (SREBP-1c), peroxisome proliferator- activated receptor-α (PPAR-α), Sirtuin 1 (SIRT1) and activating transcription factor -3 (ATF3) and the third part was used for histopathological observation.
The NAFLD rats showed marked impairment in metabolic functions associated with severe changes in the liver histological structures. The rats suffered from significant impairment in lipid metabolism and marked increase in SREBP-1c and ATF3 in liver with high elevation in the expression of miR-34a.
Propolis ethanolic extract (PEE) treatment significantly and dose-dependently improved the performance of NAFLD rats treated with different doses of PEE. PEE declined NF-κB content, SREBP-1c, ATF3 and miR-34a gene expression. PEE also significantly elevated the SIRT-1 and PPAR-α gene expression. The effect of PEE treatment was confirmed by histopathological observations.