Publication: Kuprizon ile oluşturulan multiple skleroz fare modelinde Kore ginseng kök ekstresinin nöroprotektif etkilerinin incelenmesi
Abstract
Amaç: Multiple skleroz (MS), merkezi sinir sistemini etkileyen kronik bir otoimmün hastalık olup, nöroinflamasyon ve demiyelinizasyon ile karakterizedir. Bu çalışmanın amacı, kuprizon ile indüklenen demiyelinizasyon modelinde Kore ginsengi kök ekstresinin (KGE) nöroprotektif etkilerini değerlendirmektir. Gereç ve Yöntem: C57BL/ 6 fareler; kontrol, demiyelinizasyon ve remiyelinizasyon gruplarına ayrılarak her grupta KGE tedavisi uygulanmıştır. Demiyelinizasyon, dört hafta boyunca diyete %0,2 kuprizon eklenerek indüklenmiştir. KGE (100 mg/ kg), kuprizon uygulaması sırasında veya sonrasında oral yolla verilmiştir. Çalışmada vücut ağırlığı, besin ve su alımı ile motor performans değerlendirilmiştir. Ayrıca beyin örneklerinde glutatyon (GSH), glutatyon-S-transferaz (GST), süperoksit dismutaz (SOD), malondialdehit (MDA), oligodendrosit transkripsiyon faktörü-2 (OLIG2) ve miyelin bazik protein (MBP) düzeyleri ölçülmüştür. MBP ve glial fibriller asidik protein (GFAP) ekspresyonu immünohistokimya ile değerlendirilmiş, miyelin kılıfları ise Luxol Fast Blue boyama ile incelenmiştir. Bulgular: KGE, miyelin kaybını önlemiş, remiyelinizasyonu desteklemiş ve motor performansı iyileştirmiştir. KGE tedavisi, DM grubuna kıyasla GSH, GST ve SOD düzeylerini artırmış, MDA düzeylerini ise azaltarak oksidatif stresi hafifletmiştir (p<0.05–0.001) Rotarod testinde, KGE uygulaması çubukta kalma süresi anlamlı şekilde artırmıştır (p<0.01). MBP immünreaktivitesi KGE tedavisi ile anlamlı şekilde artmıştır (skor ~2, p<0.01). Ayrıca KGE tedavisi, GFAP immünreaktivitesini azaltarak astrogliozisi baskılamış ve LFB ile değerlendirilen miyelinli alan oranını artırarak demiyelinizasyonu hafifletmiştir Sonuç: KGE, demiyelinizasyon sürecinde nöroprotektif özellikler göstermekte ve remiyelinizasyonu teşvik etmektedir. Bu bulgular, KGE'nin MS tedavisinde potansiyel bir ajan olabileceğini ortaya koymaktadır.
Objective: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system characterised by neuroinflammation and demyelination. The aim of this study was to evaluate the neuroprotective effects of Korean ginseng root extract (KGE) using a cuprizone-induced demyelination model. Materials and Methods: C57BL/ 6 mice were divided into control, demyelination and remyelination groups, with KGE treatment for each group. Demyelination was induced with 0,2% cuprizone in the diet for four weeks. KGE (100 mg/ kg) was administered by gavage during or after the cuprizone exposure. Body weight, food and water intake, and motor performance were investigated in the study. In addition, glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD) malondialdehyde (MDA), oligodendrocyte transcription factor-2 (OLIG2) and myelin basic protein (MBP) levels were measured in brain samples, while MBP and glial fibrillary acidic protein (GFAP) expression was assessed by immunohistochemistry and myelin sheaths was examined using Luxol Fast Blue staining. Results: KGE effectively prevented myelin loss, promoted remyelination, and enhanced motor performance. It significantly elevated GSH, GST, and SOD levels while reducing MDA concentrations compared to the DM group, indicating reduced oxidative stress (p<0.05 to 0.001). In the rotarod test, KGE treatment led to a significant improvement in motor endurance (p<0.01). MBP immunoreactivity was notably restored (score ~2, p<0.01). Furthermore, KGE suppressed astrogliosis by decreasing GFAP expression and alleviated demyelination by increasing LFB-positive myelinated areas. Conclusion: KGE exhibits neuroprotective properties during demyelination and promotes remyelination, highlighting its therapeutic potential for MS.
Objective: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system characterised by neuroinflammation and demyelination. The aim of this study was to evaluate the neuroprotective effects of Korean ginseng root extract (KGE) using a cuprizone-induced demyelination model. Materials and Methods: C57BL/ 6 mice were divided into control, demyelination and remyelination groups, with KGE treatment for each group. Demyelination was induced with 0,2% cuprizone in the diet for four weeks. KGE (100 mg/ kg) was administered by gavage during or after the cuprizone exposure. Body weight, food and water intake, and motor performance were investigated in the study. In addition, glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD) malondialdehyde (MDA), oligodendrocyte transcription factor-2 (OLIG2) and myelin basic protein (MBP) levels were measured in brain samples, while MBP and glial fibrillary acidic protein (GFAP) expression was assessed by immunohistochemistry and myelin sheaths was examined using Luxol Fast Blue staining. Results: KGE effectively prevented myelin loss, promoted remyelination, and enhanced motor performance. It significantly elevated GSH, GST, and SOD levels while reducing MDA concentrations compared to the DM group, indicating reduced oxidative stress (p<0.05 to 0.001). In the rotarod test, KGE treatment led to a significant improvement in motor endurance (p<0.01). MBP immunoreactivity was notably restored (score ~2, p<0.01). Furthermore, KGE suppressed astrogliosis by decreasing GFAP expression and alleviated demyelination by increasing LFB-positive myelinated areas. Conclusion: KGE exhibits neuroprotective properties during demyelination and promotes remyelination, highlighting its therapeutic potential for MS.