Serum Amiloid-A'nın Sıçanlarda Formaldehit Kaynaklı Kupffer Hücre Apoptozundaki Rolü ve Astaksantin'in Bu Süreçteki Olası Koruyucu Etkileri

Bu çalışmanın amacı Kupffer hücrelerinde formaldehit kaynaklı apoptozda Serum amiloid-A ile ilgili değişiklikleri araştırmak ve Astaksantin'in apoptoza karşı koruyucu bir etkisi olup olmadığını belirlemektir. Bu deneyde 32 sıçan 4 gruba ayrıldı (n = 8). Birinci gruba kontrol grubu adı verildi ve serum fizyolojik intraperitoneal olarak bu gruba enjekte edildi ve içme suyu oral yolla verildi. CH20 grubunda, sıçanlara günde 10 mg/kg dozda intraperitonal yoldan formaldehit enjekte edildi. CH2O+ATX16 ve CH2O+ATX32'deki gruplarındaki sıçanlara günde 10 mg/kg intraperitoneal dozda formaldehit enjekte edildi ve sırasıyla 16 mg/kg ve 32 mg/kg Astaksantin oral yolla verildi. Formaldehit uygulaması CH2O grubunda en yüksek seviyede ve istatistiksel olarakta anlamlı Serum amiloid-A boyama yoğunluğuna (P<0.0125) ve apoptotik indekse (P<0.05) neden olmuştur. Her iki dozdaki Astaksantin uygulaması Kupffer hücrelerinde apoptozu azalttı, ancak deney grupları arasında serum Serum amiloid-A düzeylerinde anlamlı bir fark yoktu (P>0.05). Sonuç olarak, oral yolla Astaksantin uygulamasının formaldehit maruziyetine bağlı olarak artan Serum Amiloid A'yı azalttığı ve muhtemelen bu şekilde Kupffer hücrelerinin formaldehit kaynaklı apoptoza karşı başarıyla koruduğu gösterilmiştir. Konu daha kapsamlı bir şekilde incelenmelidir

The Role of Serum Amyloid-A in Formaldehyde-Induced Kupffer Cell Apoptosis in Rats and Possible Protective Effects of Astaxanthin in This Process

The aim of this study is to investigate the alterations related to Serum amyloid-A in formaldehyde-induced apoptosis in Kupffer cells and to determine whether Astaxanthin has a protective effect against apoptosis. In this experiment, 32 rats were divided into 4 groups (n=8). The first group was named as control group, physiological saline was injected intraperitoneally to this group, and drinking water was given orally. In CH2O group, rats were injected with formaldehyde at a dose of 10 mg/kg daily intraperitoneally. The rats in CH2O+ATX16 and CH2O+ATX32 were injected with formaldehyde daily at a dose of 10 mg/kg intraperitoneally, and respectively 16 mg/kg and 32 mg/kg Astaxanthin were administered orally. Formaldehyde administration was caused by the highest and statistically significant Serum amyloid-A staining intensity (P<0.0125) and apoptotic index (P<0.05) in the CH2O group. Both doses of Astaxanthin administration reduced apoptosis in Kupffer cells but there were no significant differences in serum Serum amyloid-A levels between experimental groups (P>0.05). As a result, oral administration of Astaxanthin has been shown to reduce Serum Amyloid A, which increases due to exposure to formaldehyde, and possibly in this way, Kupffer cells successfully protect against formaldehyde-induced apoptosis. The subject should be examined more comprehensively

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