The expression and significance of VIP and its receptor in the cochlea of different degrees of chronic alcoholism rats.
- Author:
Jing FENG
;
Haibing LIU
- Publication Type:Journal Article
- MeSH:
Alcoholism;
metabolism;
Animals;
Cochlea;
metabolism;
Disease Models, Animal;
Down-Regulation;
RNA, Messenger;
Rats;
Rats, Sprague-Dawley;
Receptors, Vasoactive Intestinal Polypeptide, Type I;
metabolism;
Spiral Ganglion;
Vasoactive Intestinal Peptide;
metabolism
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2015;29(14):1295-1298
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To determine whether chronic alcoholism alters the expression levels of Vasoactive intestinal polypeptide (VIP) and its receptor (VIPR1) in the cochlea of chronic alcoholism rats.
METHOD:We measured their expression levels in 30 SD rats, in which we created models of different degrees of chronic alcoholism. We investigated the presence of the mRNA of VIP in the cochlea of chronic alcoholism rats and controls by reverse transcription-polymerase chain reaction (RT-PCR) method. We investigated the presence of proteins of VIPR1 in poisoned rats and controls by western blot. We also evaluated the local distribution of VIP cells by immunohistochemistry.
RESULT:We found that the levels of VIP and VIPR1 were downregulated in the chronic alcoholism groups compared to the controls group. The differences in some expression levels were significant different between chronic alcoholism rats and control rats. Moreover, at different degrees of alcohol poisoning in rats, the contents of VIP and VIPR1 differed. Decreased levels of VIP and VIPR1 were detected in the deep chronic alcoholism group compared to the group with low-degree poisoning (P < 0.05). In spiral ganglion cell plasm the expression of VIP and VIPR1 had no significant difference in three groups (P > 0.05).
CONCLUSION:These results suggest that VIP and VIPR1 play an important role in the auditory function in rats with chronic alcoholism. Chronic alcoholism may cause a peptide hormone secretion imbalance in the auditory system, eventually leading to hearing loss.
