Kronik ethanole maruz kalan sıçanların böbrek dokusunda asetil L-karnitinin endoplazmik retikulum stresi üzerine etkisi
Tarih
2023Yazar
Türk, Seval
Er, Hakan
Gemici, Ayşegül
Ercan Kelek, Sevim
Kırımlıoğlu, Esma
Üst veri
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Chronic alcohol consumption is a significant public health issue and a well-known risk factor for tissue injury. Most of the alcohol is metabolized in the liver, and a portion of ethanol is excreted unchanged through the kidneys. Cellular homeostasis, the regulation of protein synthesis, folding, and modification that govern cell growth and development, is maintained by the Endoplasmic Reticulum (ER). In the event of a disruption in this balance, Endoplasmic Reticulum Stress (ERS) is activated to restore the cell to normal conditions. Depending on the restoration of balance in ER function, ERS can lead to apoptosis or activate regenerative
pathways. Acetyl-L-carnitine (ALCAR) has the potential to be a safe and effective therapeutic compound with rare or temporary side effects. The use of ALCAR has been shown to regulate kidney functions, prevent apoptosis by increasing anti-apoptotic gene expression, and inhibit alcohol dehydrogenase activity and ethanol oxidation. However, there is insufficient research
on the effects of ALCAR administered in conjunction with chronic ethanol (CE) exposure on kidney tissue. Therefore, our study aimed to investigate the effects of ALCAR administration on ERS in kidney tissue of rats exposed to CE. In the study, 48 three-month-old rats were obtained and divided into four groups: Control group (n:12), CE group (n:12), ALCAR group
(n:12), and CE+ALCAR group (n:12). The Control group received distilled water for 4 weeks, the CE group received 5g/kg 25% ethanol, the ALCAR group received 50 mg/kg ALCAR, and the CE+ALCAR group received the same doses of ethanol+ALCAR via gavage. The localization and expression levels of ERS proteins, Grp78 and Chop, in the kidney were
demonstrated using immunohistochemistry. In the kidney tissue, compared to the C group, there was a statistically significant increase in the expression levels of GRP78 and CHOP proteins in the CE and CE+ALCAR groups. Previous studies have reported a relationship between UPR pathway and glomerular and tubular cell damage in various kidney diseases.
Our study has determined that the kidneys of rats exposed to CE are affected by the use of ALCAR in terms of ERS. The data obtained will contribute to the literature on the relationship between CE and ALCAR use with ERS and may provide a basis for future research on treatment options.