1.The changes of GAP-43 expression in spiral ganglion after exposed to noise
Yin XIA ; Haishan LONG ; Shusheng GONG ; Li LEI ; Juanjuan FENG ; Erzhong FAN ; Ying LI ; Qing ZHAO ; Demin HAN
Chinese Archives of Otolaryngology-Head and Neck Surgery 2006;0(09):-
OBJECTIVE To understand the synaptic remodel in inner ear after hearing injury by investigating growth associated protein 43(GAP-43) expression in the inner ear hair cells after exposed Kangmin mice to neural injury noise stimulation to induce permanent threshold shift(PTS) or temporary threshold shift(TTS).METHODS To compare the expressions of GAP-43 of NMDAR signal pathway during neural injury stimulation by immunocytochemistry.RESULTS The sustained GAP-43 increase occurs after 7d and 14d of PTS group,and there is not remarkable difference between them.Compared with normal control,the change is not significant in TTS group.CONCLUSION The increase of GAP-43 in spiral ganglion after 7d trauma reveals the synaptic remodel in inner ear.
2.Image-guided surgery in congenital bony aural atresia
Haishan LONG ; Demin HAN ; Haijiang DAI ; Yin XIA ; Shouqin ZHAO ; Yali ZHENG ; Jilong CHENG ; Jizhou GUO ; Guisheng WANG ; Erzhong FAN ; Ying LI
Chinese Archives of Otolaryngology-Head and Neck Surgery 2006;0(02):-
OBJECTIVE Congenital aural atresia repair is difficult owing to unpredictable anatomy. Benefits may be gained from image-guided surgery(IGS) . its exact role and surgery indication were def ined. METHODS From 2001 to 2004,36 ears with bony type C(Schuknecht classification) congenital atresia were performed. In the IGS group(n=18) ,repair surgery was performed with IGS,while in the control group(Non-IGS,n=18) ,similar intervention was applied without IGS. IGS group:aged from 12-29 years,follow-up from 6 months to 1 year. Non-IGS group:aged from 10-27 years,follow-up from 6 months to 3 years. Intra-and post-operative clinical and audiometric findings were compared. RESULTS All of the patients had congenital bony aural atresia,ossicles malformation,tympanic cavity hypoplasia and facial nerve malformation. IGS revealed a malformed horizontal semicircular canal hidden in the bony atresia plate during the operation while computed tomography(CT) did not show preoperatively. IGS computed tomography images correlated well with intra-operative findings,gave the surgeon more securityand reduced operative time(2 hours and 24 minutes) by 25 minutes. The prepare time increased 20 minutes(15-30 minutes) ,but total time decreased 5 minutes in IGS group. The registration accuracy was 0.6-1.3 mm,average 0.84 mm,which was suitable for the otologic surgery. There were 1 case in IGS group and 3 cases in Non-IGS group happened local aural restenosis after operation. But there were no facial nerve paralysis and hearing injury happened in both groups,and all of the patients got the satisfactory hearing after the hearing reconstruction(the air-bone gap with an average of IGS is 31.8dB,Non-IGS is 30.5dB) . CONCLUSION In our estimation,IGS is valuable for type C congenital aural atresia repair. It serves as an educational tool and a guide both for the experienced and inexperienced surgeons in critical situations where anatomical landmarks are distorted and approach is limited. There is no statistically significant between two groups on hearing improvement after operation.
3.The changes of phosphorylated c-Jun expression in spiral ganglion after exposed to noise.
Yin XIA ; Haishan LONG ; Demin HAN ; Shusheng GONG ; Li LEI ; Jinfeng SHI ; Erzhong FAN ; Ying LI ; Qing ZHAO
Journal of Clinical Otorhinolaryngology Head and Neck Surgery 2009;23(4):174-177
OBJECTIVE:
To investigate the mechanism of hearing pathway NMDAR regulating the changes of phosphorylated c-Jun expression in spiral ganglion after exposed Kunming mice to neural injury noise stimulation to induce permanent or temporary threshold shift.
METHOD:
To compare the different expressions of the key components (phosphorylated C-Jun) of NMDAR signal pathway during neural injury stimulation by Immunohistochemistry in CG.
RESULT:
The levels of phosphorylated c-Jun remarkably, increased in the spiral ganglion after 8 h, 48 h, 7 d and 14 d following noise trauma induced permanent threshold shift (PTS), and the numbers of positive cells reduced gradually. The similar changes occur in mice treated with MK-801 30 minutes before and after 3 h trauma induced PTS. After 48 h of noise induced TTS, the expression of Phosphorylated c-Jun return the level of normal control.
CONCLUSION
The expressions of phosphorylated c-Jun are time-related and uniform in the time and position in CG after noise trauma. MK-801 can alleviate the damage of noise trauma by altered the NMDA receptor-mediated calcium influx. Therefore, the NMDA receptors may involved in the damage of inner ear in common.
Acoustic Stimulation
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Animals
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Auditory Threshold
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Cochlea
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metabolism
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Hearing Loss, Noise-Induced
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metabolism
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JNK Mitogen-Activated Protein Kinases
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metabolism
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Mice
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Mice, Inbred Strains
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Spiral Ganglion
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metabolism
4.Expression of NR2A in rat auditory cortex after sound insulation and auditory plasticity.
Yin XIA ; Haishan LONG ; Demin HAN ; Shusheng GONG ; Li LEI ; Jinfeng SHI ; Erzhong FAN ; Ying LI ; Qing ZHAO
Journal of Clinical Otorhinolaryngology Head and Neck Surgery 2009;23(11):508-512
OBJECTIVE:
To study the changes of N-methyl-D-aspartate (NMDA) receptor subunit 2A (NR2A) expression at local synapses in auditory cortices after early postnatal sound insulation and tone exposure.
METHOD:
We prepared highly purified synaptosomes from primary auditory cortex by Optiprep flotation gradient centrifugations, and compared the differences of NR2A expression in sound insulation PND14, PND28, PND42 and Tone exposure after sound insulation for 7 days by Western blotting.
RESULT:
The results showed that the NR2A protein expression of PND14 and PND28 decreased significantly (P<0.05). Tone exposure after sound insulation for 7 days, mSIe NR2A protein level increased significantly (P<0.05). It showed bidirectional regulation of NR2A protein. No significant effects of sound insulation and lone exposure were found on the relative expression level of NR2A of PND42 (P>0.05).
CONCLUSION
The results indicate that sound insulation and experience can modify the protein expression level of NR2A during the critical period of rat postnatal development. These findings provide important data for the study on the mechanisms of the developmental plasticity of sensory functions.
Acoustic Stimulation
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Animals
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Auditory Cortex
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metabolism
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Rats
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate
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metabolism
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Synapses
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metabolism
5.Effect of Buzhong Yiqiwan on NLRP3 Inflammasome Pathway of DSS-induced Colitis Model Mice at Different Pathological Stages
Chunhui SONG ; Yihui YOU ; Junyu KE ; Geng LI ; Haishan LONG ; Yanli WU ; Qun DU ; Yanwu LI ; Wenfeng GUO
Chinese Journal of Experimental Traditional Medical Formulae 2022;28(14):20-28
ObjectiveTo explore the intervention effect and mechanism of Buzhong Yiqiwan (BZYQ) on colitis mice. MethodSixty-four C57BL/6 mice were randomly divided into 2 weeks blank group, 2 weeks model group, 2 weeks high-dose BZYQ (12 g·kg-1) group, 2 weeks low-dose BZYQ (6 g·kg-1) group, 4 weeks blank group, 4 weeks model group, 4 weeks high-dose BZYQ (12 g·kg-1) group, and 4 weeks low-dose BZYQ (6 g·kg-1) group. The colitis model was induced in mice by feeding 3% dextran sodium sulfate (DSS) for 7 days. The mice received BZYQ (12 and 6 g·kg-1) by gavage on the 8th day after modeling, once per day, and sacrificed on the 2nd and 4th weeks, correspondingly. The colon length and weight of mice in each group were measured. Hematoxylin-eosin (HE) staining was used for pathological observation and colonic mucosal inflammation was scored. The mRNA and protein expression of NOD-like receptor thermoprotein domain 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), and cysteinyl aspartate-specific protease-1 (Caspase-1) was detected by real-time quantitative polymerase chain reaction (Real-time PCR) and Western blot, respectively. Enzyme-linked immunosorbent assay (ELISA) was used to detect the content of inflammatory cytokines, such as interleukin (IL)-1β, IL-18, and IL-33 in colonic tissues. ResultCompared with the 2 weeks blank group, the 2 weeks model group showed shortened colon length, increased colon weight (P<0.05), loss of epithelial cells, destruction of gland structure, infiltration of a large number of inflammatory cells in mucosa and submucosa, local crypt abscess, and increase in mucosal inflammation score (P<0.01) as revealed by light microscopy, elevated levels of IL-1β, IL-18, and IL-33 in colonic tissues (P<0.05), and increased mRNA and protein expression of NLRP3, ASC, and Caspase-1 (P<0.05). The intervention of BZYQ (12 g·kg-1) restored colon length, alleviated mucosal injury (P<0.05), down-regulated the content of IL-18 (P<0.05), reduced the mRNA expression of NLRP3 and ASC as well as the protein expression of ASC and Caspase-1 compared with the conditions in the 2 weeks model group. Compared with the 4 weeks blank group, the 4 weeks model group showed decreased colon length, increased colon weight (P<0.05), decreased glands in the mucosal layer, expansion of glandular cavity, atrophy of crypt, local connective tissue hyperplasia and lymphocyte infiltration, increased inflammation score (P<0.01) as revealed by the light microscopy, increased expression of IL-1β, IL-18, and IL-33 (P<0.05), and elevated mRNA and expression of NLRP3 inflammasome complex (P<0.05). Compared with the conditions in the 4 weeks model group, the intervention of BZYQ (12 and 6 g·kg-1) could improve colon length and weight (P<0.05), and the intervention of BZYQ (12 g·kg-1) could also improve the inflammation score of the colon (P<0.05). Different from the acute stage, the intervention of BZYQ (12 and 6 g·kg-1) increased the content of IL-33 in the intestinal mucosa and up-regulated the mRNA and protein expression of NLRP3 inflammasome complexes ASC and Caspase-1 (P<0.05). ConclusionBZYQ can relieve the injury of colitis induced by DSS in mice. The mechanism is related to the regulation of intestinal immune response mediated by NLRP3 inflammasome, and it has different regulatory effects in acute and chronic inflammation stages.