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Objective:To explore the protective effect of α-lipoic acid (LA) on radiation damage of mice cochlear ribbon synapses.Methods:Mice were divided into five groups: control group, radiation 3 d group, radiation 3 d+ LA group, radiation 14 d group and radiation 14 d+ LA group. The radiation groups were irradiated with 16 Gy, the radiation+ LA groups were given LA once a day after radiation, the control group was given the same amount of normal saline. The auditory brainstem response (ABR) of mice were measured before irradiation and sacrifice. The number of ribbon synapses were observed with immunofluorescently labeled protein ctBP2. Western blot assay was performed to obtain the semi-quantitative expression levels of otoferlin and AP-2 protein.Results:Compared with the control group, the ABR threshold of radiation groups were significantly higher ( P<0.05) with the highest value at 14 d after irradiation ( P<0.05), and the ABR threshold of the radiation+ LA groups were significantly lower ( P<0.05). The ABR threshold shifts of 12 kHz, 24 kHz at 3 d and 14 d groups had no significant difference with 8 kHz threshold shift ( P>0.05). The 32 kHz threshold shift was significantly higher than 8 kHz threshold shift ( t=-2.38, -5.48, P<0.05). The number of ribbon synapses in the radiation groups was significantly lower than that of control group ( P<0.05), with the lowest value in the radiation 14 d group. LA treatment increased the ABR value significantly ( P<0.05). AP-2 and otoferlin protein levels were significantly reduced after irradiation, especially in the radiation 14 d groups, and they were increased by the LA treatment. Conclusions:LA has protective effect on the ribbon synapses of cochlear hair cells.
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Objective To investigate the effects of ursolic acid (UA) on cisplatin (CDDP)-induced expres_sion of transient receptor potential vanilloid 1 (TRPV1) in mouse cochlea .Methods Sixty BALB/c mice were ran_domly divided into 4 groups (15 mice in each group) and received introperitoneal injection once daily for 5 days:Control group (normol saline) ,UA group (80 mg/kg/day) ,CDDP group (4 .5 mg/kg/day) ,and CDPP (4 .5 mg/kg/day) plus UA group (80 mg/kg/day) .The expression of TRPV1 in mouse cochlea was determined by immuno_histochemistry ,microscope image analysis and western blot ,and auditory thresholds were evaluated by auditory brainstem response (ABR) measurement .ResuIts The expression of cochlea TRPV1 and ABR threshold shift was significantly increased in the mice treated with CDDP (P0 .7 , P<0 .05) .ConcIusion UA effectively attenuated CDDP -induced ototoxicity and improved auditory function through inhibition of TR_PV1 .
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ABSTRACT:Objective To investigate whether medial cerebellar nucleus may be involved in the pathogenesis of post-stroke depression (PSD)and explore the pathway that mediates this effect.Methods Healthy SD rats were randomly divided into five groups:control group,stroke group,PSD group,medial cerebellar nucleus (Med)lesion group,and superior cerebellar peduncle (xscp)lesion group.The ethological score of depression was evaluated.The neurotransmitters of Glu and GABA in the lateral hypothalamic area were detected by high performance liquid chromatography.Results Compared with those in control group,the levels of GABA and Glu expressions did not significantly differ in the lateral hypothalamic area in stroke group (P > 0.05 ).In contrast,the levels in PSD group,Med lesion group and xscp lesion group were lower than those in stroke group to different extent (P <0.01). Conclusion These results preliminarily show that medial cerebellar nucleus may participate in the pathogenesis of post-stroke depression,which may be mediated by the cerebellum-hypothalamic pathway.
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Objective To identify the role of resistin in insulin resistance(IR) by endoplasmic reticulum(ER) stress in human umbilical vein endothelial cells ( HUVECs) and in rats.Methods HUVECs were cultured in vitro and disposed by resistin (R) or tauro ursodesoxycholic acid (tudca).Expressions of GRP78, P-akt and P-eNOS were determined using Western blotting.Thoracic aortic rings were made and their dilation function exposed to different concentrations of insulin was detected.Changes of vascular morphology were observed by HE staining.Results Results of Western blotting showed that expression of GRP78 was remarkably increased,but P-akt and P-eNOS were markedly decreased in R group.However, there was no difference in expressions of GRP78, P-akt and P-eNOS between tudca group and control group.The insulin induced vasodilation was decreased in R group and there was no difference between tudca group and control.Using HE staining, the R group showed significant medial thickening and proliferation of smooth muscle.Conclusion Resistin can induce insulin resistance in vascular endothelium cells by ER stress.
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Objective To explore the mechanism of the low-frequency electrical stimulate on pedunculopontine nu-cleus to treat the Parkinson (PD) through observinge the low-frequency electrical stimulation of Pedunculopontine Nucleus (PPN) in PD rat model and the effects of neurotransmitters (GPi) neurons discharge in the medial part of the globus pallidus. Methods Thirty SD rats were randomly assigned to the control group and the PD model group, with 15 in each group. PD model was established through injecting 6-OHDA into Substantia nigra compact (SNc) of black rat. Effect of low frequency electrical stimulation, micro-electrophoresis glutamate (Glu) and its receptor blocking breaking agent MK-801,γ-aminobu-tyric acid (GABA) and its receptor antagonist bicuculline (BIC) on discharge of rat neuron GPi was examined using extracel-lular unit recording methods through seven glass microelectrode recording. Results When stimulated by low frequency electrical stimulation of PPN, reactions from the control group and neuronal response GPi in PD rats were inhibited. The aver-age discharge frequency was reduced compared to pre-stimulation (P < 0.01). Micro-electrophoresis and BIC Glu excite neurons while microiontophoresis MK-801 and GABA restrain neurons. In the background of micro-electrophoresis BIC’s excitatory effects on neuron, low-frequency electrical stimulation on PPN reduced neuronal firing frequency. And in the background of inhibition effect of micro-electrophoresis MK-801, low-frequency stimulation PPN further restrain neuronal discharge frequency. Conclusion Low frequency electrical stimulation inhibits GPi PPN neuronal activity probably though regulating neurons projecting to the Glu and GABA nerve pathways in GPi neuron.
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Objective To study the effect of high frequency stimulation (HFS) in pedunculopontine nucleus (PPN) on the neuronal activities of globus pallidus internus (Gpi) in Parkinson’s disease (PD) model rats, and the mechanisms there-of. Methods Seventy male Sprague-Dawley rats were divided into two groups, control group (n=30) and PD model group (n=40). PD rat model was established by the injection of 6-OHDA into substantia nigra pars compacta (SNc) on the right side of the brain with stereotactic technique. Electrophysiological recordings were made in anaesthetized rats to investigate the ef-fects of HFS-PPN on the firing rate of the GPi neurons. Brain microdialysis combined with high-performance liquid chroma-tography was applied to detect glutamate (Glu) andγ-aminobutyric acid (GABA) levels in GPi. Results HFS-PPN caused an excitatory reaction of the majority of neurons recorded in the GPi in PD model group and control group. The mean firing rate of GPi excited neurons was significantly increased (P﹤0.01). The levels of Glu were reduced under HFS-PPN and the levels of GABA were not affected (P>0.05).Conclusion HFS-PPN heightened the electrical activity of GPi neurons and re-duced the level of Glu. These excitatory effects were probably realized by PPN-GPi direct path or other indirect path.
