Ma T.,Peoples Hospital of Ningxia
Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery | Year: 2012
To investigate the meaning of the mutation screening, prevalence, inheritance and the intervention or the prevention for the specific drugs in 10 families with non-syndrome hearing loss in Yunnan Province, China. To do a questionnaire about the cases of ten families with non-syndrome hearing loss and to draw a detailed matriarchal family tree detailed. Following that, the A1555G mutation-positive individuals were detected and confirmed using DNA extracting, PCR amplification and sequencing for family volunteer. There are 96 members have attended the blood collection in these ten families. Thirty-six of them had the normal hearing and 60 of them had the sensory neural hearing loss. However, 4 out of those had no A1555G point mutation, and 92 had A1555G point mutation (95.8%). While 7 of those were Heterogeneity, the rest were all homogeneous mutation. There were also 73 patients who had amino glycoside antibiotic medication history. However all the rest cases had a history of amino glycoside antibiotic medication were not clear yet. The proportion of patients with drug-induced deafness is high in Yunnan province and the mutation rate of mitochondrial DNA A1555G is also high. It is worthy to do DNA 12SrRNA A1555G mutation screening for drug intervention and prevention.
Li Y.-Y.,Peoples Hospital of Ningxia |
Zhang J.-H.,Chinese Peoples Liberation Army |
Lin Y.-Z.,Dalian Medical University
Journal of Dalian Medical University | Year: 2015
Objective: To observe the change of congnitive function and the expression level of hippocampal insulin receptors (InsR) in 1 month and 3 months of diabetic rats, explore the effect of InsR on diabetic rats and investigate that whether insulin can be applied to prevent diabetic cognitive impairment. Methods: 36 healthy adult male SD (Sprague - Dawley) rats, weight 180-240 g, were divided into 3 groups randomly: diabetic group (n = 12), insulin treatment group (n = l2) and control group (re = 12), and then each group was divided into 2 groups equal in amount randomly: 1 month group and 3 months group. Diabetic group and insulin treatment group rats were induced by streptozotocin injection. Fixed time to measure blood glucose of all rats twice a week. Insulin treatment group rats were injected insulin daily, and we adjusted insulin dosage according to the blood glucose level to ensure blood glucose in normal range. All the rats underwent the test of Morris water maze in 1 month and 3 months. After the assessment on cognitive function of the 1 month and 3 months rats that experienced the Morris water maze experiment, the expression of InsR in brain were observed. Results: Compared with the control group, 1 month group of diabetic rats appeared cognitive impairment and their expression of InsR reduced, which has statistical difference (P < 0.05). Compared with 1 month diabetic group, the cognitive impairment of 3 months diabetic group was obviously aggravated and their expression of InsR reduced more significantly, which has statistical difference as well (P<0.05). 1 month group of insulin treatment rats with no significant cognitive impairment, and their expression of InsR reduced slightly. Compared with the control group, there are no difference. Compared with the 1 month diabetic group, which has statistical difference (P<0.05). 3 months group of insulin treatment rats appeared cognitive impairment and their expression of InsR reduced obviously. Compared with control group, which has statistical difference (P <0.05). Compared with 1 month group of insulin treatment rats, which has statistical difference as well (P <0. 05). Compared with 3 months group of diabetic rats, there are no statistical difference. Conclusion: Diabetic cognitive impairment is closely related to InsR, the reduced InsR expression may contribute to diabetic cognitive impairment. Early intervention of insulin has protective effect on the brain, then delay cognitive impairment. However, as the extension of the duration, the insulin treatment group rats still show cognitive impairment, which suggests that long - term application of insulin can not prevent the occurrence of cognitive impairment. Mechanisms need to be further explored.
Wang G.-H.,Nantong University |
Wang G.-H.,Fudan University |
Jiang Z.-L.,Nantong University |
Li Y.-C.,Peoples Hospital of Ningxia |
And 6 more authors.
Journal of Neurotrauma | Year: 2011
Traumatic brain injury (TBI) is one of the leading causes of neurological disability in young adults. Edaravone, a novel synthetic small-molecule free-radical scavenger, has been shown to have a neuroprotective effect in both animal models of cerebral ischemia and stroke patients; however, the underlying mechanism is poorly understood. In this report, we investigated the potential mechanisms of edaravone treatment in a rat model of TBI. TBI was induced in the right cerebral cortex of male adult rats using Feeney's weight-drop method. Edaravone (0.75, 1.5, or 3mg/kg) or vehicle (normal saline) was intravenously administered at 2 and 12h after TBI. Edaravone treatment significantly decreased hippocampal CA3 neuron loss, reduced oxidative stress, and decreased neuronal programmed cell death compared to vehicle treatment. The protective effects of edaravone treatment were also related to the pathology of TBI on non-neuronal cells, as edaravone decreased astrocyte and glial activation. Lastly, edaravone treatment significantly reduced the presence of inflammatory cytokines, cerebral edema, blood-brain barrier (BBB) permeability, and, importantly, neurological deficits following TBI. Our results suggest that edaravone exerts a neuroprotective effect in the rat model of TBI. The likely mechanism is via inhibiting oxidative stress, leading to a decreased inflammatory response and glial activation, and thereby reducing neuronal death and improving neurological function. © 2011, Mary Ann Liebert, Inc.
Chen M.-M.,Nantong University |
Zhao G.-W.,Nantong University |
He P.,Peoples Hospital of Ningxia |
Jiang Z.-L.,Nantong University |
And 6 more authors.
Journal of Ethnopharmacology | Year: 2015
Ethnopharmacological relevance "Shengyu" decoction, a traditional Chinese medicine, has been used to treat diseases with deficit in "qi" and "blood". The modified "Shengyu" decoction (MSD) used in the present study was designed to treat traumatic brain injury (TBI) on the basis of the "Shengyu" decoction, in which additional four herbs were added. Many ingredients in these herbs have been demonstrated to be effective for the treatment of brain injury. The present study was performed to evaluate the neurorestorative effect and the underlying mechanisms of MSD on the rat brain after a TBI. Materials and methods TBI was induced in the right cerebral cortex of adult rats using Feeney's weight-drop method. Intragastrical administration of MSD (1.0 ml/200 g) was begun 6 h after TBI. The neurological functions and neuronal loss in the cortex and hippocampus were determined. The levels of nerve growth-related factors GDNF, NGF, NCAM, TN-C, and Nogo-A and the number of GFAP+/GDNF+, BrdU+/nestin+, BrdU+/NeuN+ immunoreactive cells in the brain ipsilateral to TBI were also measured. Moreover, the influences of MSD on these variables were observed at the same time. Results We found that treatment with MSD in TBI rats ameliorated the neurological functions and alleviated neuronal loss. MSD treatment elevated the expression of GDNF, NGF, NCAM, and TN-C, and inhibited the expression of Nogo-A. Moreover, MSD treatment increased the number of GFAP+/GDNF+, BrdU+/nestin+, and BrdU+/NeuN+ immunoreactive cells in the cortex and hippocampus. Conclusion The present results suggest that MSD treatment in TBI rats could improve the proliferation of neural stem/progenitor cells and differentiation into neurons, which may facilitate neural regeneration and tissue repair and thus contribute to the recovery of neurological functions. These effects of modified "Shengyu" decoction may provide a foundation for the use of MSD as a prescription of medicinal herbs in the traditional medicine to treat brain injuries in order to improve the neurorestoration. © 2015 Elsevier Ireland Ltd. All rights reserved.