动物造模 z-bio 2021-07-13 267

　　Purpose: Cochlear autophagy-related proteins beclin1 and LC3, Na + -K + -2Cl- complex transporter (NKCC1) mRNA, endoserine (ET) expression, cochlear gentamicin (GM) damage and pipefenone amine hydrochloride ( PPTA) Observe relationship protection and damage mechanism.

　　Method: 60 guinea pigs were randomly divided into control group, model group, co-treatment group, post-model control group and post-treatment group. The control group received NS+perilymph, the model group received GM+perilymph, and the treatment group received GM+PPTA (both for 7 consecutive days). After modeling, the control group and the post-treatment group were continuously injected with GM for 7 days, and the perilymph and PPTA were continuously injected for 7 days. All guinea pigs were surgically implanted into the ear capsule, intraperitoneally injected with NS and GM (160mg? Kg-1? D-1), and the ear capsule was injected with perilymph and PPTA. After the treatment of each group of guinea pigs, the hearing was analyzed by ABR test, and the expressions of beclin 1 and LC3, NKCC1 mRNA and ET-1 were detected.

　　Results: The ABR results of the model group and the post-model control group were not significantly different (P→0.05), but they were all significantly higher than the other three groups (Pu003c0.05). The ABR threshold of the guinea pigs in the proportional simultaneous treatment group was significantly lower than that of the late treatment group (Pu003c0.05). After modeling, the expressions of LC3II and Beclin1 in the model group were significantly higher than those of the other four groups, and the expressions of LC3II and Beclin1 in the late treatment group were lower than those in the control group. The expression of NKCC1 mRNA in the model group was higher than that of the other groups4. The expression of NKCC1 mRNA in the treatment group was equivalent to that of the control group after model establishment (Pu003c0.05). The expression of ET-1 in each part of the model group was significantly higher than that of the other 4 groups. The expression of ET-1 in each part of the control group was lower than the other 4 groups. After modeling, the ET-1 of each part of the treatment group was lower than that of the control group.

　　Conclusion: PPTA inhibits the expression of cochlear autophagy NKCC1 and ET-1, thereby protecting the cochlea from gentamicin damage. PPTA is more effective against gentamicin cochlear damage in the early stage, indicating that transgene may cause effective irreversible damage. Auditory cells.