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157 results on '"Lin, Dingkun"'

8. Microenvironment‐Responsive Injectable Conductive Hydrogel for Spinal Cord Injury Repair.

Author

Liu, Qi, Wang, Wanshun, Yang, Haimei, Wang, Yingjie, Shi, Yingdi, Chen, Youlin, Luo, Dan, Guo, Da, Lin, Dingkun, Yue, Kan, and Li, Xing

Abstract

Spinal cord injury (SCI) represents a severe neurological condition often coupled with a drastic secondary inflammatory response, which further exacerbates the damage in most cases. Due to their unique electrical and mechanical compatibilities with the spinal cord, the utilization of conductive hydrogels through injection for SCI repair, particularly in scenarios involving non‐uniform and large gaps, has emerged as a promising approach. Herein, leveraging the acidic microenvironment characteristic of acute SCI sites, an injectable conductive hydrogel with pH‐responsive immunoregulation is engineered for SCI repair. Based on the dynamic Schiff base chemistry and covalent photo‐crosslinking, this composite hydrogel, composed of gelatin methacryloyl, oxidized dextran, and MoS2, exhibits adjustable mechanical and conductive properties, enabling a customized match with the natural spinal cord's attributes. Additionally, the incorporation of Wnt5a and its selective release in acidic conditions prompt the immediate suppression of inflammatory factors and enhances neural differentiation and regeneration. In the 2‐mm hemisection mouse SCI model, the optimized conductive hydrogel can effectively bridge the injury gap, establish nerve connections and signal, mitigate inflammatory response, and promoted recovery of mobility. This novel injectable conductive hydrogel system offers a promising advance in therapeutic materials for SCI repair. [ABSTRACT FROM AUTHOR]

Published
2024
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10. Injectable, Electroconductive, Free Radical Scavenging Silk Fibroin/Black Phosphorus/Glycyrrhizic Acid Nanocomposite Hydrogel for Enhancing Spinal Cord Repair

Author

Zhang, Beichen, primary, Wang, Wanshun, additional, Gao, Peng, additional, Li, Xiang, additional, Chen, Lingling, additional, Lin, Zefeng, additional, Chen, Hu, additional, Liang, Wenhao, additional, Kong, Zhiyuan, additional, Lin, Dingkun, additional, Wu, Xiaona, additional, and Zhang, Tao, additional

Published
2024
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13. Chronic ACLD Knees with Early Developmental Cartilage Lesions Exhibited Increased Posterior Tibial Translation during Level Walking.

Author

Zeng, Xiaolong, Lin, Fangzheng, Huang, Wenhan, Kong, Lingchuang, Zeng, Jiajun, Guo, Da, Zhang, Yu, and Lin, Dingkun

Subjects
KNEE pain, ANTERIOR cruciate ligament, MOTION capture (Human mechanics), CARTILAGE cell transplantation, MENISCUS (Anatomy), CARTILAGE, KNEE, ARTICULAR cartilage
Abstract

Objective: Early articular cartilage lesion (CL) is a vital sign in the onset of posttraumatic knee osteoarthritis (PTOA) in patients with anterior cruciate ligament deficiency (ACLD). Researchers have suggested that altered kinematics could accelerate CLs and, therefore, lead to the onset of PTOA. However, little is known about whether specific knee kinematics exist that lead to early CL in chronic ACLD knees. Level walking is the most frequent and relevant in vivo activity, which greatly impacts knee health. We hypothesized that the knee kinematics during level walking in chronic ACLD knees with early tibiofemoral CL would significantly differ from those of chronic ACLD knees without early tibiofemoral CL. Methods: Thirty patients with a chronic ACLD history, including 18 subjects with CLs and 12 subjects without CLs, and 35 healthy control subjects were recruited for the study from July 2020 to August 2022. The knee kinematic data during level walking were collected using a three‐dimensional motion analysis system. The kinematic differences between groups were compared using statistical parametric mapping with one dimension for One‐Way ANOVA. The cartilage statuses of the ACLD knees were assessed via MRI examination. The CLs distribution of subjects was evaluated using a modified Noyes scale and analyzed by chi‐square tests. Results: ACLD knees with CLs had significantly greater posterior tibial translation (7.7–8.0mm, 12%–18% gait cycle GC, p = 0.014) compared to ACLD knees without CLs during level walking. ACLD knees with CLs had greater posterior tibial translation (4.6–5.5mm, 0%–23% GC, p < 0.001; 5.8–8.0mm, 86%–100% GC, p < 0.001) than healthy controls during level walking. In the group of ACLD knees with CLs, CL is mainly located in the back of the tibia plateau and front of load bearing area of the medial femoral condyle (p < 0.05). Conclusion: Chronic anterior cruciate ligament deficient knees with cartilage lesions have increased posterior tibial translation compared to anterior cruciate ligament deficient knees without cartilage lesions and healthy subjects. The posterior tibial translation may play an important role in knee cartilage degeneration in ACLD knees. The increased posterior tibial translation and cartilage lesion characteristics may improve our understanding of the role of knee kinematics in cartilage degeneration and could be a helpful potential reference for anterior cruciate ligament deficient therapy, such as physical training to improve abnormal kinematic behavior. [ABSTRACT FROM AUTHOR]

Published
2024
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19. Polydatin administration attenuates the severe sublesional bone loss in mice with chronic spinal cord injury

Author

Zhan, Jiheng, primary, Luo, Dan, additional, Zhao, Bingde, additional, Chen, Shudong, additional, Luan, Jiyao, additional, Luo, Junhua, additional, Hou, Yu, additional, Hou, Yonghui, additional, Xu, Wenke, additional, Yan, Wanying, additional, Qi, Ji, additional, Li, Xing, additional, Zhang, Qing, additional, and Lin, Dingkun, additional

Published
2022
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26. Inhibitory Effects of Rhaponticin on Osteoclast Formation and Resorption by Targeting RANKL-Induced NFATc1 and ROS Activity

Author

He, Jianbo, primary, Chen, Kai, additional, Deng, Tiancheng, additional, Xie, Jiewei, additional, Zhong, Kunjing, additional, Yuan, Jinbo, additional, Wang, Ziyi, additional, Xiao, Zhifeng, additional, Gu, Ronghe, additional, Chen, Delong, additional, Li, Xiaojuan, additional, Lin, Dingkun, additional, and Xu, Jiake, additional

Published
2021
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33. Sodium tanshinone IIA sulfonate promotes spinal cord injury repair by inhibiting blood spinal cord barrier disruption in vitro and in vivo.

Author

Luo, Dan, Li, Xing, Hou, Yonghui, Hou, Yu, Luan, Jiyao, Weng, Jiaxian, Zhan, Jiheng, and Lin, Dingkun

Subjects
SPINAL cord injuries, SPINAL cord, CORD blood, ADHERENS junctions, SODIUM, TIGHT junctions
Abstract

Spinal cord injury (SCI) leads to microvascular damage and the destruction of the blood spinal cord barrier (BSCB), which can progress into secondary injuries, such as apoptosis and necrosis of neurons and glia, culminating in permanent neurological deficits. BSCB restoration is the primary goal of SCI therapy, although very few drugs can repair damaged barrier structure and permeability. Sodium tanshinone IIA sulfonate (STS) is commonly used to treat cardiovascular disease. However, the therapeutic effects of STS on damaged BSCB during the early stage of SCI remain uncertain. Therefore, we exposed spinal cord microvascular endothelial cells to H2O2 and treated them with different doses of STS. In addition to protecting the cells from H2O2‐induced apoptosis, STS also reduced cellular permeability. In the in vivo model of SCI, STS reduced BSCB permeability, relieved tissue edema and hemorrhage, suppressed MMP activation and prevented the loss of tight junction and adherens junction proteins. Our findings indicate that STS treatment promotes SCI recovery, and should be investigated further as a drug candidate against traumatic SCI. [ABSTRACT FROM AUTHOR]

Published
2022
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39. Coenzyme Q10 suppresses oxidative stress and apoptosis via activating the Nrf-2/NQO-1 and NF-κB signaling pathway after spinal cord injury in rats

Author

Li, Xing, Zhan, Jiheng, Hou, Yu, Chen, Shudong, Hou, Yonghui, Xiao, Zhifeng, Luo, Dan, and Lin, Dingkun

Subjects
Original Article
Abstract

Spinal cord injury (SCI) is one of the most devastating diseases that may cause paralysis, disability and irreversible loss of functions, which ultimately lead to permanent disabilities and a decrease in patient life expectancy. Coenzyme Q10 (CoQ10) is a lipid-soluble vitamin-like benzoquinone compound that can exert antioxidant and anti-apoptotic functions in a variety of diseases. However, the antioxidant and anti-apoptotic effects of CoQ10 in the treatment of SCI are still unknown. Therefore, we designed experiments to measure the changes in antioxidant capacity (glutathione (GSH), superoxide dismutase (SOD) and the end product of lipid peroxidation (MDA)) and apoptosis products (Bax, Bcl-2 and Caspase-3) to evaluate the protective effects of CoQ10 on SCI and investigated whether CoQ10 exerts its functions through the Nrf-2/NQO-1 and NF-κB signaling pathway. Our results showed that CoQ10 treatment could significantly decrease the levels of oxidative products (MDA) and increase the activities of antioxidant enzymes (SOD and GSH) against oxidative stress, as well as decrease the levels of pro-apoptotic proteins (Bax and Caspase-3) and increase the levels of anti-apoptotic proteins (Bcl-2) against apoptosis after SCI. We also observed that CoQ10 exerted beneficial effects through the Nrf-2/NQO-1 and NF-κB signaling pathway. These findings suggested that CoQ10 had a protective effect by decreasing oxidative stress and apoptosis after SCI. Thus, our data may provide a new approach wherein CoQ10 may be considered as a potential effective therapeutic for the treatment of SCI.

Published
2019

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