盐酸椒苯酮胺 z-bo 2020-11-11 377

　　Objective: To observe the relationship between guinea pig cochlear autophagy-related proteins beclin1 and LC3, Na+-K+-2Cl- combined transporter (NKCC1) mRNA, endothelin (ET) expression and cochlear gentamicin (GM) damage and piperphentonamine hydrochloride (PPTA) The protective effect and mechanism of injury.

　　Method: 60 guinea pigs were randomly divided into a control group, a model group, a concurrent treatment group, a post-model control group, and a post-treatment group. The control group was given NS+artificial perilymph, the model group was given GM+artificial perilymph, and the treatment group was given GM+PPTA (both continuously administered for 7 days). After the model was established, the control group and the post-treatment group were given continuous injection of GM for 7 days. Then, artificial perilymph and PPTA were injected continuously for 7 days. All guinea pigs were treated with ear vesicles before administration, NS and GM (160 mg·kg-1·d-1) were injected intraperitoneally, and artificial perilymph and PPTA were injected with ear vesicles. After the guinea pigs of each group finished the administration, the hearing was analyzed by ABR test, and the expression of beclin1 and LC3, NKCC1 mRNA and ET-1 were detected.

　　Results: There was no significant difference in ABR results between the model group and the control group after modeling (P>0.05), but both were significantly higher than the other three groups (P<0.05). The ABR threshold of the guinea pigs in the treatment group was significantly lower than that in the later stage Treatment group (P<0.05); the expression of LC3Ⅱ and Beclin1 in the model group was significantly higher than that of the other 4 groups, and the expression of LC3Ⅱ and Beclin1 in the later treatment group was lower than that of the control group after modeling; the expression of NKCC1 mRNA in the model group was higher than that of the other 4 groups Significantly higher (P<0.05), and the expression of NKCC1 mRNA in the post-treatment group was significantly lower than that in the control group after modeling (P<0.05). 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 that of the other 4 groups. The expression of ET-1 in each part of the treatment group was lower than that of the control group after modeling.

　　Conclusion: PPTA can inhibit the expression of cochlear cell autophagy, NKCC1 and ET-1, thereby protecting the cochlea from gentamicin injury; PPTA is more effective against gentamicin cochlear injury in the early stage, suggesting that GM may affect auditory cells Produce irreversible damage.