Assessment of the protective and therapeutic effect of melatonin against thioacetamide‐induced acute liver damage

Abstract

Acute or chronic damage to the liver may occur through alcohol, drugs, viruses, genetic disorders, and toxicity. In this study, we planned to investigate the protective and therapeutic effects of melatonin (Mel) by causing damage to the liver with thioacetamide (TAA). Thirty‐five rats were used. Group I: control group (seven pieces), group II: Mel group (seven pieces) the single dose on the first day of the experiment was 10 mg/kg, group III: TAA (seven pieces) 300 mg/kg with 24‐hour intervals, two doses, group IV: Mel + TAA group (seven pieces) 10 mg/kg single dose Mel was applied 24 hours before TAA application, group V: TAA + Mel group (seven pieces) single dose (24th hour) of 10 mg/kg Mel was administered after TAA (300 mg/kg) two doses. The liver histology was evaluated. Apoptosis, autophagy, and necrosis markers in tissue were determined by immunohistochemistry. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) levels in blood serum samples and transforming growth factor‐β (TGF‐β) and tumor necrosis factor‐α (TNF‐α) levels were determined in liver tissue. TAA affected histologically the classical lobule structure both in cell cords and sinusoids. Caspase‐3, RIP3, and LC3 levels were increased in group III compared with the control group. TAA did not cause a statistically significant change in TNF‐α level but decreased the TGF‐β level significantly. AST and ALT levels were statistically significant in group II and V compared with group I, the ALP level was significant in group IV compared with group II. The results of this study showed that TAA caused significant damage to tissues and increased cell death, Mel was found to have more therapeutic than the protective effect on tissues.

Thymoquinone attenuates doxorubicin‐cardiotoxicity in rats

“…Sections were stained with Hematoxylin‐Eosin (H&E), photographs were taken with an light microscope (Olympus BX51, Center Valley, PA). [ 14 ]…”

Melatonin Mitigates Cisplatin-Induced Ovarian Dysfunction via Altering Steroidogenesis, Inflammation, Apoptosis, Oxidative Stress, and PTEN/PI3K/Akt/mTOR/AMPK Signaling Pathway in Female Rats

“…However, co-treatment of melatonin and cisplatin, rats exhibited a positive PAS and increased PAS optical density in zona pellucida and oocyte. The previous study showed that melatonin, although by a small amount, corrected thioacetamide, it caused depletion of liver glycogen storage according to PAS staining [54]. The distribution of glycogen density was found to be increased in the bisphenol A and melatonin compared to the bisphenol-A only treated rats [55].…”

Karbon Tetraklorürün Neden Olduğu Akciğer Hasarında L-Karnitinin Antiapoptotik ve Histopatolojik Değişiklikler Üzerindeki Rolü

“…Yine CCl4 ile yapılan çalışmalarda CCl4'ün kaspaz enzim sistemini aktive ederek apoptozu arttırdığı ve böylece doku hasarına yol açtığı bildirilmiştir (8,25). Başka bir maddeyle karaciğer hasarının indüklendiği bir çalışmada kaspaz-3 pozitif hepatositlerin sayısı hasar oluşturulan grupta yüksek bulunmuştur (26). Akciğer dokusunda yapılan çalışmaları incelediğimizde ise, CCl4 ile oluşturulan akciğer hasarında kaspaz-3 enzim aktivitesi diğer gruplardan yüksek bulunmuştur (8).…”