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| 1 | Effects of Xinfeng capsule on pulmonary function based on treg-mediated notch pathway in a rat model of adjuvant arthritis显示文摘OBJECTIVE:To observe the impact of xinfeng xapsule(XFC) on pulmonary function in a rat model of adjuvant arthritis(AA) and to investigate the mechanism of action.METHODS:Forty rats were randomly divided into four groups of ten:normal control(NC);model control(MC);tripterygium glycosides tablet(TPT);and xinfeng capsule(XFC).Except for the NC group,AA was induced in all rats by intracutaneous injection of 0.1 mL Freund's complete adjuvant in the right paw on the 19th day.NC and MC groups were given(0.9%) physiological saline.The TPT and XFC groups were given TPT(10 mg/kg) and XFC(1.2 g/kg),respectively.Thirty days after administration,changes in paw edema(E),the arthritis index(AI),pulmonary function,levels of regulatory T-cells(Treg),ultrastructure of lung tissue,and expression of Notch receptors and ligands in lung tissue were observed.RESULTS:In the MC group,E and the AI were increased and pulmonary function significantly decreased;the structure of alveolar type-II cells was damaged;ratios of Treg in peripheral blood were reduced;and expression of Notch receptors such as Notch3 and Notch4 and ligands such as Delta1 in lung tissue were significantly increased whereas expression of Notch1,Jagged1 and Jagged2 were significantly decreased.After intervention with XFC,E and the AI were decreased;pulmonary function was enhanced;the structure of alveolar type-II cells was improved;and expression of Treg,Notch1,Jagged1,Jagged2 was elevated,whereas that of Notch3,Notch4 and Delta1 was reduced.CONCLUSION:XFC can not only inhibit E and the AI and improve joint symptoms,it can also improve pulmonary function and reduce inflammation in lung tissue.These actions could be carried out through increases in the expression of Treg,Notch receptors(Notch1) and ligands(Jagged1,Jagged2),and reductions in the expression of Notch3,Notch4 and Delta1.These phenomena would reduce the deposition of immune complexes and the inflammatory response in lung tissue,thereby improving joint symptoms and pulmonary function. | Lei Wan Jian Liu Chuanbing Huang Yuan Wang Xi Shen Wandong Zhang Guizheng Wang Haixia Fan Yao Ge Ruilian Chen Yunxiang Cao Ruikai Zong Li Lei | 2012 | Journal of Traditional Chinese Medicine2012，32，3： | 17 |
| 2 | Fine mapping of a major flowering time QTL on soybean chromosome 6 combining linkage and association analysis显示文摘 | Dan Zhang Hao Cheng Zhenbin Hu Hui Wang Guizheng Kan Chunying Liu Deyue Yu | 2013 | Euphytica2013，，1： | 1 |
| 3 | Ultrasensitive immunoassay based on anodic near-infrared electro- chemiluminescence from dual-stabilizer-capped CdTe nanocrystals 显示文摘 | LIANG Guodong LIU Shufeng ZOU Guizheng | 2012 | Anal Chem2012，84，10： | 1 |
| 4 | Immunostaining of chymase in the mast cell in human dystrophic skeletal muscle显示文摘 | Guizheng Z | 1997 | J Aichi Med Univ1997，25，19： | 1 |
| 5 | Risk of metabolic abnormalities in osteoarthritis:a new perspective to understand its pathological mechanisms显示文摘Although aging has traditionally been viewed as the most important risk factor for osteoarthritis(OA),an increasing amount of epidemiological evidence has highlighted the association between metabolic abnormalities and OA,particularly in younger individuals.Metabolic abnormalities,such as obesity and typeⅡdiabetes,are strongly linked to OA,and they affect both weightbearing and non-weight-bearing joints,thus suggesting that the pathogenesis of OA is more complicated than the mechanical stress induced by overweight.This review aims to explore the recent advances in research on the relationship between metabolic abnormalities and OA risk,including the impact of abnormal glucose and lipid metabolism,the potential pathogenesis and targeted therapeutic strategies. | Guizheng Wei Ke Lu Muhammad Umar Zhenglin Zhu William WLu John RSpeakman Yan Chen Liping Tong Di Chen | 2023 | Bone Research2023，11，4： | 0 |
| 6 | miR-204 ameliorates osteoarthritis pain by inhibiting SP1-LRP1 signaling and blocking neuro-cartilage interaction显示文摘Osteoarthritis(OA)is a painful degenerative joint disease and is the leading cause of chronic disability among elderly individuals.To improve the quality of life for patients with OA,the primary goal for OA treatment is to relieve the pain.During OA progression,nerve ingrowth was observed in synovial tissue and articular cartilage.These abnormal neonatal nerves act as nociceptors to detect OA pain signals.The molecular mechanisms for transmitting OA pain in the joint tissues to the central nerve system(CNS)is currently unknown.MicroRNA miR-204 has been demonstrated to maintain the homeostasis of joint tissues and have chondro-protective effect on OA pathogenesis.However,the role of miR-204 in OA pain has not been determined.In this study,we investigated interactions between chondrocytes and neural cells and evaluated the effect and mechanism of miR-204 delivered by exosome in the treatment of OA pain in an experimental OA mouse model.Our findings demonstrated that miR-204 could protect OA pain by inhibition of SP1-LDL Receptor Related Protein 1(LRP1)signaling and blocking neuro-cartilage interaction in the joint.Our studies defined novel molecular targets for the treatment of OA pain. | Ke Lu Qingyun Wang Liuzhi Hao Guizheng Wei Tingyu Wang William WLu Guozhi Xiao Liping Tong Xiaoli Zhao Di Chen | 2023 | Bioactive Materials2023，，8： | 0 |
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