scholarly journals P310 MOLECULAR MECHANISM OF THE CHONDRO-PROTECTIVE EFFECTS OF INTRAARTICULAR INJECTIONS WITH HYLAN G-F 20 IN A RABBIT MODEL OF OSTEOARTHRITIS

2006 ◽  
Vol 14 ◽  
pp. S169
Author(s):  
P. Li ◽  
D. Raitcheva ◽  
E. Hutto ◽  
M. Hawes ◽  
X. Yu ◽  
...  
2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Yang Chen ◽  
Haijun Li ◽  
Xiaochao Luo ◽  
Huahui Liu ◽  
Yumei Zhong ◽  
...  

Rheumatoid arthritis (RA) is a systemic and chronic autoimmune inflammatory disease characterized by severe synovial hyperplasia associated with progressive cartilage degradation. Due to the severe pain and disability caused by RA, effective therapeutic strategies that could simultaneously alleviate the inflammatory response and delay the disease progression are urgently needed. As a major alternative therapy in traditional Chinese medicine, moxibustion has been demonstrated that it could reduce the chronic inflammatory responses of a series of musculoskeletal diseases; however, whether moxibustion has protective effects on RA is still unclear. To investigate the effects of moxibustion on RA, moxibustion was applied to Zusanli (ST36) and Shenshu (BL23) acupoints in a RA rabbit model. HE staining of articular cartilage showed that moxibustion alleviated the cartilage degradation and bone destruction. In addition, moxibustion decreased the osteoclast number in RA rabbits. Real-time PCR revealed that moxibustion decreased the expression of RANKL mRNA while increased the expression of OPG mRNA, indicating a restoration of the balance between osteogenesis and osteoclastogenesis. Taken together, our results indicated that moxibustion had promising antiarthritic effects and could be an useful alternative method in RA therapeutics.


2016 ◽  
Vol 10 (3) ◽  
pp. 036010
Author(s):  
Yong-Jian Ma ◽  
Hou-De Zhang ◽  
Chuang-Hong Wu ◽  
Guo-Liang Zhu ◽  
Yong-Qiang Ji ◽  
...  

2020 ◽  
Vol 21 (3) ◽  
pp. 704 ◽  
Author(s):  
Dmitry V. Chistyakov ◽  
Viktoriia E. Baksheeva ◽  
Veronika V. Tiulina ◽  
Sergei V. Goriainov ◽  
Nadezhda V. Azbukina ◽  
...  

Ocular inflammation contributes to the pathogenesis of blind-causing retinal degenerative diseases, such as age-related macular degeneration (AMD) or photic maculopathy. Here, we report on inflammatory mechanisms that are associated with retinal degeneration induced by bright visible light, which were revealed while using a rabbit model. Histologically and electrophysiologically noticeable degeneration of the retina is preceded and accompanied by oxidative stress and inflammation, as evidenced by granulocyte infiltration and edema in this tissue, as well as the upregulation of total protein, pro-inflammatory cytokines, and oxidative stress markers in aqueous humor (AH). Consistently, quantitative lipidomic studies of AH elucidated increase in the concentration of arachidonic (AA) and docosahexaenoic (DHA) acids and lyso-platelet activating factor (lyso-PAF), together with pronounced oxidative and inflammatory alterations in content of lipid mediators oxylipins. These alterations include long-term elevation of prostaglandins, which are synthesized from AA via cyclooxygenase-dependent pathways, as well as a short burst of linoleic acid derivatives that can be produced by both enzymatic and non-enzymatic free radical-dependent mechanisms. The upregulation of all oxylipins is inhibited by the premedication of the eyes while using mitochondria-targeted antioxidant SkQ1, whereas the accumulation of prostaglandins and lyso-PAF can be specifically suppressed by topical treatment with cyclooxygenase inhibitor Nepafenac. Interestingly, the most prominent antioxidant and anti-inflammatory benefits and overall retinal protective effects are achieved by simultaneous administrating of both drugs indicating their synergistic action. Taken together, these findings provide a rationale for using a combination of mitochondria-targeted antioxidant and cyclooxygenase inhibitor for the treatment of inflammatory components of retinal degenerative diseases.


Pancreas ◽  
2013 ◽  
Vol 42 (1) ◽  
pp. 102-107 ◽  
Author(s):  
Yan Lu ◽  
Yanmei Yu ◽  
Meilan Yang ◽  
Hui Liu ◽  
Bin Li ◽  
...  

2021 ◽  
Author(s):  
Yanmei Zhang ◽  
yuan yao ◽  
Runxiu Zhu ◽  
Niyang Aida ◽  
Jun Yuan ◽  
...  

Abstract Background Vascular dementia (VD) is a kind of clinical syndrome characterized with the impairment cognitive function caused by cerebrovascular disease. Genetics, biochemical, and morphological analyses of cell and animal models, reveal that mitochondria could have roles in this neurodegeneration. Methods We used Sprague-Dawley rats to establish VD model, and used the proteomics method based on relative quantification (iTRAQ) to identify the differentially expressed proteins in hippocampus mitochondria. Results A total of 33 differentially expressed proteins were identified between the VD rats and the VD rats treated with nerve growth factor groups. And five differentially expressed proteins (Rgs14, Slc7a14, Ppm1l, Kcnj10 and Syngr1) were identified after completing the sham-operate control, VD rats and VD rats treated with nerve growth factor groups, then successfully confirmed by western blot. Bioinformatics analysis suggested that the mitochondrial molecular mechanism of VD and the protective effect of nerve growth factor on mitochondrial function of VD rats may be due to different molecular mechanisms. Conclusion We estimated that mitochondrial dysfunction may be the onset of VD and key role in the pathological process of VD. This study not only has a deeper understanding of the mitochondrial molecular mechanism of VD, but also is helpful for the screening of drug targets.


2021 ◽  
Author(s):  
Petra Kollárová-Brázdová ◽  
Olga Lencova-Popelova ◽  
Galina Karabanovich ◽  
Júlia Kocúrová-Lengvarská ◽  
Jan Kubes ◽  
...  

The anthracycline (ANT) anticancer drugs such as doxorubicin or daunorubicin (DAU) can cause serious myocardial injury and chronic cardiac dysfunction in cancer survivors. A bisdioxopiperazine agent dexrazoxane has been developed as a cardioprotective drug to prevent these adverse events, but it is uncertain whether it is the best representative of the class. This study used a rabbit model of chronic ANT cardiotoxicity to examine another bisdioxopiperazine compound called GK-667, a water-soluble prodrug of ICRF-193, as a potential cardioprotectant. The cardiotoxicity was induced by DAU (3 mg/kg, i.v. weekly, 10 weeks), and GK-667 (1 or 5 mg/kg, i.v.) was administered before each DAU dose. The treatment with GK-667 was well tolerated and provided full protection against DAU-induced mortality and left ventricular (LV) dysfunction (determined by echocardiography and LV catheterization). Markers of cardiac damage/dysfunction revealed minor cardiac damage in the group co-treated with GK-667 in the lower dose, whereas almost full protection was achieved with the higher dose. This was associated with similar prevention of DAU-induced dysregulation of redox and calcium homeostasis proteins. GK-667 dose-dependently prevented p53-mediated DNA damage response in the LV myocardium not only in the chronic experiment but also after single DAU administration. These effects appear essential for cardioprotection, presumably because of the topoisomerase IIβ inhibition provided by its active metabolite ICRF-193. In addition, GK-667 administration did not alter the plasma pharmacokinetics of DAU and its main metabolite daunorubicinol in rabbits in vivo. Hence, GK-667 merits further investigation as a promising drug candidate for cardioprotection against chronic ANT cardiotoxicity.


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