d 半乳糖诱导拟老化大鼠内耳中线粒体外膜易位酶tom40 tom20及线粒体内膜易位酶tim23的表达研究word格式论文.docxVIP

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d 半乳糖诱导拟老化大鼠内耳中线粒体外膜易位酶tom40 tom20及线粒体内膜易位酶tim23的表达研究word格式论文.docx

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d 半乳糖诱导拟老化大鼠内耳中线粒体外膜易位酶tom40 tom20及线粒体内膜易位酶tim23的表达研究word格式论文

ABSTRACTObjective: To investigate the role of mitochondrial protein import in the mechanism of presbycusis.Methods: Ninety six female Wistar rats at 1 month of age were randomly divided into four groups, each of which contains twenty four rats. Group B, C and D were treated with subcutaneous administration of 150mg/kg, 300mg/kg and 500mg/kg dose of hypodermic D-galactose respectively for eight weeks, meanwhile group A were treated with the same dose of saline as control group. Auditory brainstem response (ABR) was used to detect the hearing threshold of each rat in all four groups before and after the 8 weeks injection treatment. The mtDNA 4834 bp deletion of inner ear tissue was detected by real-time PCR technique. The mRNA expression levels of tom40, tom20 and tim23 in the inner ear was examined by real-time RT-PCR technique. The protein levels of tom40, tom20 and tim23 was measured by western blot.Results: The difference in elevation of ABR threshold among the four groups was not significant (p0.05). The mtDNA 4834 bp deletion rates of group B, C and D were significantly higher(9.16%±0.32%, 11.65%±0.58%, 15.09%±0.94% respectively) compared with group A(3.91%±0.33%)(p0.05), and the difference among group B, group C and group D was also significant (p0.05). The differences of mRNA expression levels of tom40, tom20 and tim23 among all groups were not significant (p0.05).The differences of protein levels of tom40 and tom20 between all the other groups were all significant (p0.05), except between group A and B (p0.05). However, the difference of protein levels of tim23 between all groups was not significant (p0.05).Conclusion: The protein levels of tom40 and tom20 decreased in the inner ear of mimetic aging rat induced by D-galactose. It indicated that the dysfunction of mitochondrial protein import and translocation system components may be extensively involved in the aging of the inner ear, which may cause the disorder of the translocation of nuclear-encoded