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Your search keyword '"Xu, Zucai"' showing total 170 results
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170 results on '"Xu, Zucai"'

10. A multicenter, randomized, open‐label, phase 2 clinical study of telitacicept in adult patients with generalized myasthenia gravis

Author

Yin, Jian, primary, Zhao, Mingming, additional, Xu, Xianhao, additional, Zhang, Meini, additional, Xu, Zucai, additional, Li, Zunbo, additional, Qin, Xinyue, additional, Li, Zhuyi, additional, Zhao, Chongbo, additional, Zhou, Hongyu, additional, Ma, Ying, additional, Cao, Wenfeng, additional, Wang, Guoping, additional, Lin, Yongzhong, additional, Zhang, Jizhong, additional, Zhang, Xu, additional, Cai, Hongbin, additional, Qian, Weidong, additional, Wang, Yiqi, additional, Zhang, Xinghu, additional, Liu, Guangzhi, additional, Wang, Jiawei, additional, Qiu, Wei, additional, Min, Lianqiu, additional, Li, Jing, additional, Deng, Hui, additional, Chu, Lan, additional, Zhang, Yifan, additional, and Fang, Jianmin, additional

Published
2024
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13. The mechanism of mitochondrial autophagy regulating Clathrin‐mediated endocytosis in epilepsy.

Author

Zhou, Xuejiao, Yang, Yu, Tai, Zhenzhen, Zhang, Haiqing, Yang, Juan, Luo, Zhong, and Xu, Zucai

Subjects
PARKIN (Protein), INTRACELLULAR space, EXTRACELLULAR fluid, EPILEPTIFORM discharges, PROTEIN expression, ENDOCYTOSIS
Abstract

Objective: The objective of this study is to determine whether inhibition of mitophagy affects seizures through Clathrin‐mediated endocytosis (CME). Methods: Pentylenetetrazol (PTZ) was intraperitoneally injected daily to establish a chronic PTZ‐kindled seizure. The Western blot (WB) was used to compare the differences in Parkin protein expression between the epilepsy group and the control group. Immunofluorescence was used to detect the expression of MitoTracker and LysoTracker. Transferrin‐Alexa488 (Tf‐A488) was injected into the hippocampus of mice. We evaluated the effect of 3‐methyladenine (3‐MA) on epilepsy behavior through observation in PTZ‐kindled models. Results: The methylated derivative of adenine, known as 3‐MA, has been extensively utilized in the field of autophagy research. The transferrin protein is internalized from the extracellular environment into the intracellular space via the CME pathway. Tf‐A488 uses a fluorescent marker to track CME. Western blot showed that the expression of Parkin was significantly increased in the PTZ‐kindled model (p < 0.05), while 3‐MA could reduce the expression (p < 0.05). The fluorescence uptake of MitoTracker and LysoTracker was increased in the primary cultured neurons induced by magnesium‐free extracellular fluid (p < 0.05); the fluorescence uptake of Tf‐A488 was significantly decreased in the 3‐MA group compared with the control group (p < 0.05). Following hippocampal injection of Tf‐A488, both the epilepsy group and the 3‐MA group exhibited decreased fluorescence uptake, with a more pronounced effect observed in the 3‐MA group. Inhibition of mitophagy by 3‐MA from day 3 to day 9 progressively exacerbated seizure severity and shortened latency. Significance: It is speculated that the aggravation of seizures by 3‐MA may be related to the failure to remove damaged mitochondria in time and effectively after inhibiting mitochondrial autophagy, affecting the vesicle endocytosis function of CME and increasing the susceptibility to epilepsy. Summary: Abnormal mitophagy was observed in a chronic pentylenetetrazol‐induced seizure model and a Mg2+‐free‐induced spontaneous recurrent epileptiform discharge model. A fluorescent transferrin marker was utilized to track clathrin‐mediated endocytosis. Using an autophagy inhibitor (3‐methyladenine) on primary cultured neurons, we discovered that inhibition of autophagy led to a reduction in fluorescent transferrin uptake, while impairing clathrin‐mediated endocytosis function mediated by mitophagy. Finally, we examined the effects of 3‐methyladenine in an animal model of seizures showing that it exacerbated seizure severity. Ultimately, this study provides insights into potential mechanisms through which mitophagy regulates clathrin‐mediated endocytosis in epilepsy. [ABSTRACT FROM AUTHOR]

Published
2024
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37. Inhibition of STAT3 signal pathway recovers postsynaptic plasticity to improve cognitive impairment caused by chronic intermittent hypoxia.

Author

Wang, Jin, Xu, Zucai, Xu, Ling, and Xu, Ping

Abstract

Purpose: Chronic intermittent hypoxia (CIH) is a major cause of cognitive dysfunction in people with obstructive sleep apnea syndrome (OSAS), as it damages synapse structure, and function. This study aimed to investigate the potential mechanisms resulting in cognitive impairment caused by CIH in patients with OSAS. Methods: Healthy adult SD male rats (n = 36) were randomly divided into four groups: control, CIH, WP1066, and dimethyl sulfoxide (DMSO). The CIH, WP1066, and DMSO groups were exposed to intermittent hypoxic environments for 8 h per day for 28 d. The WP1066 group received intraperitoneal injection of WP1066, a selective signal transducer and activator of transcription-3 (STAT3) inhibitor. All the experimental rats were subjected to the Morris water maze. Hippocampal tissue samples (n = 6 per group) were used for western blot analysis, and brain tissue samples (n = 3 per group) were used for immunohistochemistry and hematoxylin and eosin staining. Results: The cognition of rats exposed to prolonged CIH was impaired. P-STAT3 expression was found to be higher in CIH rats than in control rats. Postsynaptic density95 (PSD95) expression was significantly reduced in rats with CIH-induced learning and memory impairment, but it significantly increased after the STAT3 signaling pathway was blocked, which improved learning and memory ability. However, inhibition of the STAT3 signaling pathway failed to improve the decline of synaptophysin (SYP) protein caused by CIH. Conclusions: When rats are exposed to CIH, STAT3 in the brain is activated, PSD95 and SYP levels decrease, and cognition is impaired. Inhibition of the STAT3 signaling pathway increases PSD95 to recover postsynaptic plasticity, thereby improving cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Published
2023
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43. Gut Microbes Regulate Innate Immunity and Epilepsy

Author

Zhang, Linhai, Li, Shuang, Tai, Zhenzhen, Yu, Changyin, and Xu, Zucai

Subjects
General Neuroscience
Abstract

Epilepsy is a common chronic brain disease. There are many clinical methods to control epileptic seizures, such as anti-seizure medications (ASMs) or surgical removal of epileptogenic lesions. However, the pathophysiology of epilepsy is still unknown, making it difficult to control or prevent it. The host’s immune system monitors gut microbes, interacts with microbes through pattern recognition receptors such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs) expressed by innate immune cells, and activates immune responses in the body to kill pathogens and balance the relationship between microbes and host. In addition, inflammatory responses induced by the innate immune system are seen in animal models of epilepsy and temporal lobe epilepsy brain tissue to combat pathogens or injuries. This review summarizes the potential relationship between gut microbes, innate immunity, and epilepsy based on recent research to provide more hints for researchers to explore this field further.

Published
2022

47. Gut Microbial Characteristics of Adult Patients With Epilepsy

Author

Dong, Lian, primary, Zheng, Qian, additional, Cheng, Yongran, additional, Zhou, Mengyun, additional, Wang, Mingwei, additional, Xu, Jianwei, additional, Xu, Zucai, additional, Wu, Guofeng, additional, Yu, Yunli, additional, Ye, Lan, additional, and Feng, Zhanhui, additional

Published
2022
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