Person:
ŞAHİN, ALİ

Profile Picture

Email Address

Birth Date

Research Projects

Organizational Units

OrgUnit Logo
Organizational Unit

Job Title

Last Name

ŞAHİN

First Name

ALİ

Name

Filters

2018 - 201912020 - 20211
Reset filters

Settings

Author: SÖZEN, AHMET ERDİ × Subject: OXIDATIVE STRESS ×

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    PublicationOpen Access
    High Cholesterol Diet-Induced Changes in Oxysterol and Scavenger Receptor Levels in Heart Tissue
    (HINDAWI LTD, 2018-06-13) SÖZEN, AHMET ERDİ; Sozen, Erdi; Yazgan, Burak; Sahin, Ali; Ince, Umit; Ozer, Nesrin Kartal
    Involvement of high cholesterol and oxidative stress in cardiovascular diseases is well studied, as it can be hypothesized that various products originated from lipid peroxidation, such as oxysterols, or affected protein expression might lead to cardiomyocyte damage followed by the pathological modifications. Although oxidation of excessive cholesterol to oxysterols in elevated stress conditions is identified by a number of studies, the role of a high cholesterol diet in regulating fatty acid and oxysterol accumulation, together with scavenger receptor mRNA levels, in the heart remains little investigated. Our study provides a detailed analysis of the changes in fatty acid, oxysterol, and scavenger receptor profiles and its relation with histological alterations in the heart tissue. We evaluated alterations of fatty acid composition, by the GC-MS method, while 4 beta-, 25-, and 27-hydroxycholesterol and 7-ketocholesterol levels by means of LC-MS/MS in high cholesterol diet-fed rabbits. Additionally, a number of proteins related to lipid metabolism and scavenger receptor mRNA expressions were evaluated by Western blotting and RT-PCR. According to our in vivo results, a high cholesterol diet enhances a number of unsaturated fatty acids, oxysterols, and LXR alpha, in addition to CD36, CD68, CD204, and SR-FI expressions while alpha-tocopherol supplementation decreases LXR alpha and SR expressions together with an increase in 27-hydroxycholesterol and ABCA1 levels. Our results indicated that the high cholesterol diet modulates proteins related to lipid metabolism, which might result in the malfunction of the heart and alpha-tocopherol shows its beneficial effects. We believe that this work will lead the generation of different theories in the development of heart diseases.
  • No Thumbnail Available
    PublicationMetadata only
    alpha-Tocopherol supplementation reduces inflammation and apoptosis in high cholesterol mediated nonalcoholic steatohepatitis
    (WILEY, 2021) SÖZEN, AHMET ERDİ; Demirel-Yalciner, Tugce; Sozen, Erdi; Ozaltin, Esra; Sahin, Ali; Ozer, Nesrin Kartal
    Inflammation and apoptosis signaling are crucial steps in the progression from nonalcoholic fatty liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH). Alpha-tocopherol, the most active form of vitamin E, is an important modulator of signaling mechanisms, but its involvement to cholesterol-induced NASH pathogenesis remains poorly defined. Herein we have reported a novel effect of alpha-tocopherol in the transition from hepatic steatosis to NASH. High cholesterol diet alone (without alpha-tocopherol) in rabbits elevated NASH development as indicated by increased inflammatory response, apoptotic activity and liver fibrosis. Such elevation results from induction of signaling mechanisms since the expressions of IL1 beta, phospho c-Jun/c-Jun ratio, JNK, caspase 9, CHOP and Bax were increased, and recruitment of macrophage, alpha-smooth muscle actin (alpha-SMA) and COL1A1 into the liver tissue were induced. Alpha-tocopherol supplementation inhibited inflammatory response, apoptosis and fibrosis development without affecting lipid accumulation in high cholesterol-induced NASH. Specifically, alpha-tocopherol lowered the inflammatory level as observed by reduced macrophage infiltration and JNK/c-Jun signaling. Lower inflammatory status co-occurred with the reduction of CHOP and Bax expressions as well as fibrosis-related COL1A1 and alpha-SMA levels. Taken together, alpha-tocopherol supplementation inhibits cholesterol-induced NASH development by lowering JNK/c-Jun/inflammation axis in addition to JNK/CHOP/apoptosis signaling, which might contribute to resistance against NAFLD/NASH transition.