تاثير يك دوره تمرين استقامتي بر ميزان بيان ژن هاي PRDX6 و KAT2B در هيپوكمپ موش هاي صحرايي آلزايمري شده با آميلوئيد بتا: يك مطالعه تجربي

The Effect of Endurance Training on the Expression of PRDX6 and KAT2B Genes in Hippocampus of Beta Amyloid-Induced Rat Model of Alzheimer's Disease: An Experimental Study

زﻣﯿﻨﻪ و ﻫﺪف: ﺑﯿﻤﺎري آﻟﺰاﯾﻤﺮ راﯾﺞﺗﺮﯾﻦ ﺷﮑﻞ زوال ﻋﻘﻞ اﺳﺖ. (Lysine Acetyltransferase 2B) KAT2B ﯾﮏ ﭘﺮوﺗﺌﯿﻦ ﻣﯿﺘﻮﮐﻨﺪرﯾﺎﯾﯽ اﺳﺖ ﮐﻪ ﺑﻪ ﻋﻨﻮان ارﮔﺎن ﮐﻨﺘﺮلﮐﻨﻨﺪه ﭘﺎكﺳﺎزي ﻣﯿﺘﻮﮐﻨﺪري ﺗﻮﺳﻂ ﻣﯿﺘﻮﻓﺎژي ﺷﻨﺎﺧﺘﻪ ﺷﺪه اﺳﺖ. PRDX6 )6 Peroxiredoxin( ﺗﻨﻈﯿﻢﮐﻨﻨﺪه ﮐﻠﯿﺪي ﻣﯿﺘﻮﻓﺎژي اﺳﺖ و ﻧﻘﺶ ﺣﯿﺎﺗﯽ در ﺣﻔﻆ ﻫﻤﻮﺳﺘﺎز Reactive oxygen species) ROS( ﻣﯿﺘﻮﮐﻨﺪري اﯾﻔﺎء ﻣﯽﮐﻨﺪ. ﺑﻨﺎﺑﺮاﯾﻦ ﻫﺪف از ﭘﮋوﻫﺶ ﺣﺎﺿﺮ ﺗﻌﯿﯿﻦ ﺗﺄﺛﯿﺮ ﺗﻤﺮﯾﻦ اﺳﺘﻘﺎﻣﺘﯽ ﺷﻨﺎ ﺑﺮ ﻣﯿﺰان ﺑﯿﺎن ژنﻫﺎي PRDX6 و KAT2B در ﻫﯿﭙﻮﮐﻤﭗ ﻣﺪل ﻣﻮش ﺻﺤﺮاﯾﯽ ﻧﺮ ﻧﮋاد وﯾﺴﺘﺎر ﭘﺲ از اﻟﻘﺎء آﻟﺰاﯾﻤﺮ ﻣﯽﺑﺎﺷﺪ. ﻣﻮاد و روشﻫﺎ: در ﻣﻄﺎﻟﻌﻪ ﺗﺠﺮﺑﯽ ﺣﺎﺿﺮ، 18 ﺳﺮ ﻣﻮش ﺻﺤﺮاﯾﯽ ﺑﻪ ﺻﻮرت ﺗﺼﺎدﻓﯽ ﺑﻪ 3 ﮔﺮوه ﮐﻨﺘﺮل، آﻟﺰاﯾﻤﺮ و ﮔﺮوه ﺗﻤﺮﯾﻦ-آﻟﺰاﯾﻤﺮ ﺗﻘﺴﯿﻢ ﺷﺪﻧﺪ. ﻣﺪل آﻟﺰاﯾﻤﺮ ﺑﺎ ﺗﺰرﯾﻖ آﻣﯿﻠﻮﺋﯿﺪ ﺑﺘﺎ1-42 ﺑﻪ ﻣﻨﻄﻘﻪ CA1 ﻫﯿﭙﻮﮐﻤﭗ اﯾﺠﺎد ﺷﺪ و ﻣﻮشﻫﺎي ﺻﺤﺮاﯾﯽ ﮔﺮوه ﺗﻤﺮﯾﻨﯽ ﺑﻪ ﻣﺪت 3 ﻫﻔﺘﻪ، ﻫﺮ روز و ﺑﻪ ﻣﺪت 30 دﻗﯿﻘﻪ در ﺗﻤﺮﯾﻦ ﺷﻨﺎ ﺷﺮﮐﺖ ﮐﺮدﻧﺪ. ﺑﻪ ﻣﻨﻈﻮر ﺗﺄﯾﯿﺪ ﻣﺪل آﻟﺰاﯾﻤﺮ از رﻧﮓآﻣﯿﺰي ﺗﯿﻮﻓﻼوﯾﻦ و ﺑﺮاي ﺗﻌﯿﯿﻦ ﻣﯿﺰان ﺑﯿﺎن ژنﻫﺎي ﻣﻮرد ﻧﻈﺮ از روشReal Time PCR اﺳﺘﻔﺎده ﺷﺪ. ﺑﺮاي ﺗﺠﺰﯾﻪ و ﺗﺤﻠﯿﻞ دادهﻫﺎ از آﻧﺎﻟﯿﺰ وارﯾﺎﻧﺲ ﯾﮏ ﻃﺮﻓﻪ و آزﻣﻮن ﺗﻌﻘﯿﺒﯽ Tukey اﺳﺘﻔﺎده ﺷﺪ. ﯾﺎﻓﺘﻪﻫﺎ: ﺑﯿﻦ ﻣﯿﺰان ﭘﻼكﻫﺎي ﺑﺘﺎ آﻣﯿﻠﻮﺋﯿﺪ در دو ﮔﺮوه آﻟﺰاﯾﻤﺮ و ﮐﻨﺘﺮل ﺗﻔﺎوت ﻣﻌﻨﯽدار وﺟﻮد داﺷﺖ )0/001

Alzheimer's disease is the most common form of dementia. KAT2B (Lysine Acetyltransferase 2B) is a mitochondrial protein known as mitochondria clearing control organ by mitophagy. PRDX6 (Peroxiredoxin 6) is a key regulator of mitophagy and plays a critical role in maintaining mitochondrial ROS (Reactive oxygen species) homeostasis. Therefore, the purpose of this study was to investigate the effect of swimming endurance training on expression of PRDX6 and KAT2B genes in male hippocampus model of Wistar rat after induction of Alzheimer's. Materials and Methods: In this experimental study, 18 rats were randomly divided into 3 groups including control, Alzheimer's and exercise-Alzheimer's groups. The Alzheimer's model was created by injecting beta 42-1 amyloid into the CA1 hippocampus region, and the training group rats participated in the swimming 30 min/day for a period of 3 weeks. In order to confirm the Alzheimer's model, thioflavin staining was used, and Real Time PCR method was used to determine the expression of the desired genes. One-way ANOVA with Tukey’s post-hoc test was used for data analysis. Results: There was a significant difference between the amount of beta-amyloid plaques in the two groups of Alzheimer's and control (p<0.001). Alzheimer's disease significantly reduced the expression of PRDX6 and KAT2B genes in the Alzheimer's rats hippocampus (p<0.001), and also following the endurance exercise, the PRDX6 gene expression increased compared with the Alzheimer's group (p=0.027). Conclusion: Endurance training can possibly maintain oxidative balance and improve mitochondrial hemostasis in Alzheimer's disease.