Songül BENZİGÜL, Saliha Ayşenur CAM, Fatma UYSAL, Seyfullah Oktay ARSLAN, Hayriye TATLI DOĞAN

Arı Sütünün Amiloid Beta ile Deneysel Alzheimer Modeli Oluşturulmuş Sıçanlarda Etkileri

Giriş: Arı sütünün amiloid beta1-42 enjekte edilerek Alzheimer modeli oluşturulan sıçanlarda, bilişsel işlevin azalmasına ve sinir hücresi inflamasyonuna karşı doza bağlı etkisini araştırmayı amaçladık. Yöntemler: Çalışmada, 35 adet 4 aylık 280-310 g ağırlığında Wistar-Albino erkek sıçan kullanıldı. Her grupta 7 sıçan olacak şekilde 5 grup oluşturuldu. Aβ1-42, hamilton mikroenjektörü ile hipokampüse çift taraflı 4µg/taraf enjekte edildi. Kontrol grubuna Aβ1-42 yerine, aynı miktarda serum fizyolojik enjekte edildi. Hipokampüs içine Aβ1-42 uygulamasından önceki 7 gün ve sonraki 10 günden sonra, arı sütü sıçan gruplarına sırasıyla 30 mg/kg, 100 mg/kg, 300 mg/kg mide sondası ile uygulandı. Bu uygulamalar bittikten sonra iki gün sürecek olan Pasif Sakınma testi, sonra beş gün sürecek olan Morris Su Tankı deneyleri uygulandı. Hipokampüs dokularında TNF-α ve IL-1β düzeyleri ölçüldü. İmmünohistokimyasal incelemelerde GFAP ve Iba1 boyanma şiddeti ve yaygınlığı, ayrıca astroglia ve mikroglia hücrelerinin aktive olmuş morfolojiye sahip olup olmamaları esas alındı. Bulgular: Gruplar karşılaştırıldığında, pasif sakınma testi ve morris su tankı testleri uygulanan sıçanlarda Aβ1-42 uygulamasıyla öğrenme ve hafızada gerileme oluştu. Arı sütü 30 mg/kg, 100 mg/kg ve 300 mg/kg uygulamasında öğrenme ve hafızada oluşan gerilemenin geri dönüşünde istatistiksel anlamlılık elde edilemedi. Alzheimer hastalığı grubunda gözlenen astrosit ve mikroglia aktivite artışının, 30 mg/kg grubu hariç diğer tedavi gruplarında baskılandığı görüldü. Hipokampüste TNF-α ve IL-1β düzeylerinin, Aβ1-42 uygulaması ile arttığı görüldü ve tedavi gruplarında arı sütü 30 mg/kg grubu hariç diğer iki grupta (100 ve 300 mg/kg) bu artışın baskılandığını tespit edildi. Sonuç: Alzheimer modellememizdeki bulgularımıza göre arı sütü uygulaması sonucu, oluşan astoglial ve mikroglial aktivite ve inflamasyon yapıcı sitokin artışının baskılandığı görülmüştür.

Effects of royal jelly on rats with amyloid beta in experimental Alzheimer's model

Objective: The aim of this study was to evaluate the dose-dependent effect of royal jelly against reduction of cognitive function and neuroinflammation in rats that were injected with amyloid beta1-42 peptide in Alzheimer's model. Methods: In the study, 35 4-month-old Wistar-Albino male rats weighing 280-310 g were used. 5 groups were formed with 7 rats in each group. The Aβ1-42 peptide was injected 4µg/side to be bilateral into the hippocampus with the Hamiltonian microinjector. The control group was injected with the same amount of saline, instead of Aβ1-42 7 days before and 10 days after Aβ1-42 administration into the hippocampus, royal jelly was administered to the rat groups at doses of 30 mg/kg 100 mg/kg, and 300 mg/kg, respectively, by gastrıc gavaj. After these applications were completed, the Passive Avoidance test, which would last for two days, and then the Morris Water Tank experiments, which would last for five days, were applied. TNF-α and IL-1β levels were measured in the hippocampus tissues. For the evaluation of immunohistochemical staining for immunohistochemical examinations, the severity and extent of staining for GFAP and Iba1, and whether astroglia and microglia cells have activated morphology were taken as basis. Results: When the groups were compared, there was a decline in learning and memory with the application of Aβ1-42 in rats undergoing Passive Avoidance test and Morris Water Tank tests. After administration of royal jelly doses of 30 mg/kg, 100 mg/kg and 300 mg/kg, there was no improvement in learning and memory decline. The increase in astrocyte and microglia activity observed in the Alzheimer's disease group was suppressed in treatment groups with other doses, except for the as 30 mg/kg group. TNF-α and IL-1β levels in the hippocampus were increased with the administration of Aβ1-42 peptide, and we found that this increase was suppressed in the treatment groups in the other two groups (100 and 300 mg/kg), except for the dose group of royal jelly 30 mg/kg. Conclusion: According to our findings in our Alzheimer's model, the application of royal jelly was found to suppress the resulting astoglial and microglial activity and inflammatory cytokine increase.

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