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目的探讨Na-K-2Cl联合转运子1(Na-K-2Cl cotransporter1,NKCC1)和α2Na,K-ATP酶(α2Na,K-AT-Pase)在血管纹性老年性聋(strial presbycusis)发病过程中的作用。方法分别以不同基因型的NKCC1小鼠(杂合子和野生型)和α2Na,K-ATPase小鼠(杂合子和野生型)为实验对象,检测小鼠生长过程不同阶段的听性脑干反应(auditory brainstem response,ABR)和耳蜗内电位(endocochlear potential,EP),以观察NKCC1和α2Na,K-ATPase基因缺陷与血管纹性老年性聋的关系。结果听性脑干反应检测结果显示,与NKCC1+/+野生型小鼠相比较,NKCC1+/-杂合子小鼠的ABR阈值在所有周龄组的各测试频率均升高,差异均有统计学意义(均P<0.05)。NKCC1+/-杂合子小鼠的听力随鼠龄增长而下降,与低龄小鼠相比,老龄小鼠的ABR阈值显著升高(均P<0.05)。NKCC1+/-小鼠的EP也随年龄增长而呈下降趋势,老龄小鼠的EP值与低龄小鼠相比明显降低(P<0.05)。α2Na,K-ATPase+/-杂合子小鼠的听力及EP低于同周龄组野生型小鼠,其听力随鼠龄增长而下降,高龄小鼠的ABR阈值与其低龄时相比明显升高(P<0.05)。结论只携带1个NKCC1或α2Na,K-ATPase等位基因的小鼠(杂合子)可呈现伴EP下降的年龄相关性听力下降,耳蜗侧壁的NKCC1和α2Na,K-ATPase基因缺陷可能在血管纹性老年性聋的发病中起一定作用。
Objective To investigate the role of Na-K-2Cl cotransporter1 (NKCC1) and α2Na, K-ATPase (α2Na, K-AT-Pase) in the pathogenesis of strial presbycusis In the role. Methods The NKCC1 mice (heterozygous and wild type) and α2Na, K-ATPase mice (heterozygous and wild type) with different genotypes were used as experimental subjects to detect the auditory brainstem response in different stages of mouse growth (ABR) and endocochlear potential (EP) in order to observe the relationship between NKCC1, α2Na and K-ATPase gene defects and vascular dementia in senile deafness. Results The results of auditory brainstem response showed that compared with NKCC1 + / + wild type mice, the ABR threshold of NKCC1 +/- heterozygous mice increased at all test frequencies in all week groups, with statistical significance (All P <0.05). The hearing ability of NKCC1 +/- heterozygous mice decreased with increasing age, and the ABR threshold of aged mice was significantly higher than that of the younger mice (all P <0.05). The EP of NKCC1 +/- mice also showed a decreasing trend with age, and the EP value of aged mice was significantly lower than that of the younger mice (P <0.05). α2Na, K-ATPase +/- heterozygous mice hearing and EP lower than the wild-type mice of the same age group, the hearing decreased with the increase of age, ABR threshold in old mice was significantly higher than their younger age P <0.05). CONCLUSIONS: Age-associated hearing loss in individuals with only one NKCC1 or α2Na, K-ATPase allele may be associated with age-related hearing loss associated with EP decline. Defects in the NKCC1 and α2Na, K-ATPase genes in the cochlear sidewall may be localized in the blood vessels The impact of age-related deafness plays a role.