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6 results on '"Weicheng Qin"'

1. Restoring bone-fat equilibrium: Baicalin's impact on P38 MAPK pathway for treating diabetic osteoporosis

Author

Weicheng Qin, Qi Shang, Gengyang Shen, Bing Li, Peng Zhang, Yuzhuo Zhang, Wenhua Zhao, Honglin Chen, Huiwen Liu, Bin Xie, Zhida Zhang, Hui Ren, and Xiaobing Jiang

Subjects
Baicalin, Diabetic osteoporosis, P38-MAPK, Bone-fat equilibrium, Osteogenesis, Adipogenesis, Therapeutics. Pharmacology, RM1-950
Abstract

Diabetes can lead to a disorder of bone-fat balance, a significant cause of osteoporosis due to changes in environmental factors. Baicalin (Bai), an active ingredient of Scutellaria baicalensis, has been confirmed to possess antioxidant, hypoglycemic, and anti-osteoporotic effects. However, a comprehensive understanding of Bai's influence on diabetic osteoporosis (DOP), including its effects and underlying mechanisms, remains elusive. This study investigated Bai's impact on the bone-fat equilibrium in rats with DOP. The results indicated that Bai alleviated bone damage in DOP by promoting osteogenesis and inhibiting adipogenesis. Concurrently, through bioinformatics analysis, it was suggested that Bai's mechanism of action might involve the P38-MAPK pathway. In vitro, Bai was found to enhance the development of bone marrow mesenchymal stem cells (BMSCs) towards osteogenic lineages while suppressing their differentiation towards adipogenic lineages. It was discovered that Bai's promotion of BMSC osteogenic differentiation depends on the P38-MAPK pathway. Additionally, the synergistic effect mediated by Bai and P38-MAPK inhibitor suppressed BMSC adipogenic differentiation. Our research indicates that the P38-MAPK pathway play a role in Bai's effects on the osteogenic-adipogenic differentiation of BMSCs, showcasing the potential for DOP treatment. This study highlights Bai's ability to regulate the equilibrium between bone and fat, presenting a novel approach to adressing DOP.

Published
2024
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2. Potential molecular targets and drugs for basement membranes-related intervertebral disk degeneration through bioinformatics analysis and molecular docking

Author

Zelin Zhou, Weicheng Qin, Peng Zhang, Jiahui He, Zhaojun Cheng, Yan Gong, Guangye Zhu, De Liang, Hui Ren, Xiaobing Jiang, and Yuping Sun

Subjects
Basement membranes, Annulus fibrosus, Intervertebral disc degeneration, Bioinformatic analysis, Molecular docking, Diseases of the musculoskeletal system, RC925-935
Abstract

Abstract Background Through bioinformatics analysis to identify the hub genes of Intervertebral disc degeneration (IVDD) associated with basement membranes (BMs) and find out the potential molecular targets and drugs for BMs-related annulus fibrosus (AF) degeneration based on bioinformatic analysis and molecular approach. Methods Intervertebral disc degeneration (IVDD) related targets were obtained from GeneCards, DisGenet and OMIM databases. BMs related genes were obtained from Basement membraneBASE database. The intersection targets were identified and subjected to protein-to-protein interaction (PPI) construction via STRING. Hub genes were identified and conducted Gene ontology (GO) and pathway enrichment analysis through MCODE and Clue GO in Cytospace respectively. DSigDB database was retrieved to predict therapeutic drugs and molecular docking was performed through PyMOL, AutoDock 1.5.6 to verify the binding energy between the drug and the different expressed hub genes. Finally, GSE70362 from GEO database was obtained to verify the different expression and correlation of each hub gene for AF degeneration. Results We identified 41 intersection genes between 3 disease targets databases and Basement membraneBASE database. PPI network revealed 25 hub genes and they were mainly enriched in GO terms relating to glycosaminoglycan catabolic process, the TGF-β signaling pathway. 4 core targets were found to be significant via comparison of microarray samples and they showed strong correlation. The molecular docking results showed that the core targets have strong binding energy with predicting drugs including chitosamine and retinoic acid. Conclusions In this study, we identified hub genes, pathways, potential targets, and drugs for treatment in BMs-related AF degeneration and IVDD.

Published
2023
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3. Traumatic asymmetrical bilateral hip dislocation: A rare case report

Author

Weicheng Qin and Yue Fang

Subjects
musculoskeletal diseases, Male, medicine.medical_specialty, medicine.medical_treatment, Joint Dislocations, Avascular necrosis, Case Report, Manual reduction, Fracture Fixation, Internal, Fractures, Bone, Fracture fixation, medicine, Internal fixation, Hip Dislocation, Humans, Orthopedics and Sports Medicine, Joint dislocation, Reduction (orthopedic surgery), Asymmetrical hip dislocation, business.industry, Rehabilitation, Acetabulum, Middle Aged, medicine.disease, Surgery, trauma, Heterotopic ossification, business, traumatic hip dislocation
Abstract

Traumatic bilateral hip dislocation is a rare phenomenon. Simultaneous traumatic asymmetrical bilateral hip dislocation is even more unusual. There is no report in the literature regarding the mechanism of injury in tramcar squeezing. A 49-year-old male who had a serious tramcar accident and developed asymmetric bilateral hip dislocations (left posterior, right anterior) combined with fracture of left acetabulum and multiple injuries was admitted. Right hip dislocation was treated with manual reduction. Left hip dislocation, fracture of acetabulum and bilateral pubis, and open wound of left thigh were treated with open reduction and internal fixation. In conclusion, hip dislocation should be performed with manual reduction within 6 h. If manual reduction fails, open reduction and even internal fixation can be performed to prevent complications, such as avascular necrosis of the femoral and heterotopic ossification.

Published
2021

4. Jingui Shenqi Pills Regulate Bone-Fat Balance in Murine Ovariectomy-Induced Osteoporosis with Kidney Yang Deficiency

Author

Kai Tang, Hui Ren, De Liang, Wenhua Zhao, Weicheng Qin, Zhida Zhang, Qi Shang, Jingjing Tang, Xiaobing Jiang, Honglin Chen, Fuyong Yu, Juanmin Li, Xiang Yu, Xuan Huang, Guifeng Chen, and Gengyang Shen

Subjects
medicine.medical_specialty, Article Subject, Osteoporosis, Bone morphogenetic protein 2, 03 medical and health sciences, chemistry.chemical_compound, Other systems of medicine, 0302 clinical medicine, Internal medicine, Adipocyte, medicine, Protein kinase B, PI3K/AKT/mTOR pathway, 030304 developmental biology, 0303 health sciences, Kidney, business.industry, Osteoblast, medicine.disease, FNDC5, medicine.anatomical_structure, Endocrinology, Complementary and alternative medicine, chemistry, 030220 oncology & carcinogenesis, business, RZ201-999, Research Article
Abstract

Jingui Shenqi Pills (JGSQP) have been a staple of traditional Chinese medicine for thousands of years, used primarily as a treatment for kidney yang deficiency (KYD). In vitro analyses of JGSQP revealed strong induction of osteogenic differentiation and inhibition of adipogenic differentiation in bone-marrow-derived mesenchymal stem/stromal cells. However, the mechanisms by which JGSQP regulate the bone-fat balance in murine ovariectomy-induced osteoporosis with KYD have not been reported. Materials and Methods. Two-month-old female C57BL/6 mice were divided randomly into three groups: those receiving a sham operation (Sham); those undergoing bilateral ovariectomy and selection of KYD syndrome (Model); and those subjected to both bilateral ovariectomy and KYD syndrome selection for 8 weeks, followed by JGSQP treatment for 4 weeks (JGSQP). In the Sham and Model groups, mice were given the same dose of distilled water orally for 4 weeks. Animals from all three groups were euthanised at the 12th week. Vertebral microarchitecture and histomorphology were examined by micro-CT and H&E staining, respectively. In addition, we examined the mRNA expression of Akt, Wnt10b, Osterix (Osx), Fndc5, PPARγ, and Fabp4, as well as the protein of AKT, phosphorylation-AKT (p-AKT), BMP2, COL1A1, and FNDC5. Results. JGSQP treatment improved bone microarchitecture and mitigated histomorphological damage relative to the Model group. The osteoblast number (Ob.N/BS) and area (Ob.S/BS) were increased, whereas adipocyte number (adipocyte/tissue area) and area (adipocyte area/tissue area) were decreased in the JGSQP group. JGSQP treatment reduced the mRNA expression of Akt and adipogenesis-related genes (Fndc5, PPARγ, and Fabp4) while promoting osteogenesis-related genes (Wnt10b and Osx) mRNA expression. Additionally, the expression of p-AKT, BMP2, and COL1A1 proteins was increased and FNDC5 protein expression was decreased after JGSQP treatment. Conclusions. JGSQP treatment reversed murine ovariectomy-induced osteoporosis with KYD by controlling bone-fat balance via AKT pathway.

Published
2020

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