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The incidence of cartilage degeneration (osteoarthritis, etc.) is increasing year by year, putting heavy pressure on families and society. It has become a consensus that mesenchymal stem cells can repair damaged cartilage. As the research progresses, more and more evidence indicates that its effects are attributed to the paracrine system, especially the exosomes. Exosomes are a lipid bilayer cystic structure encapsulating biologically active factors such as proteins, lipids, mRNA, and microRNAs (miRNAs/miRs), which can regulate the biological functions of cells. As a signal and carrier for transmitting important information between cells, it plays a very important role in the repair of cartilage degeneration damage. This paper reviews the research of mesenchymal stem cell-derived exosomes carrying miRNAs in the repair of cartilage injury.
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<p><b>OBJECTIVE</b>To investigate the inhibitory effect of tetramethylpyrazine (Tet) preconditioning on overload training-induced myocardial apoptosis in rats, and to explore cardioprotective mechanisms of Tet preconditioning.</p><p><b>METHODS</b>A total of 25 male Sprague-Dawley rats were randomly divided into three groups, including the control group (n=5), the overload training group (overload training for 8 weeks, n=10), and the Tet preconditioning group (Tet preconditioning for 8 weeks before overload training, n=10). After 8 weeks, cardiac structure and myocardial apoptosis were analyzed by histology, transmission electron microscopy, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay staining. The expressions of Bcl-2, Bax, Caspase-3, and Caspase-9 in myocardium were evaluated by immunohistochemical staining.</p><p><b>RESULTS</b>Overload training caused swelling, disorder, partial rupture, and necrosis of myocardial focal necrotic fibers, as well as mitochondrial vacuolization, cristae rupturing, and blurring. In contrast, Tet preconditioning attenuated the swelling of myocardial fibers, decreased the amount of ruptured fibers, and inhibited mitochondrial vacuolization, resulting in clear cristae. Overload training significantly increased Bax expression and decreased Bcl-2/Bax ratio when compared with the control group (P<0.01). Conversely, Tet preconditioning significantly increased Bcl-2 expression and the Bcl-2/Bax ratio as compared with the overload training group (P<0.05). Overload training dramatically increased the expressions of Caspase-3 and Caspase-9 when compared with the control groupP<0.05). Following Tet preconditioning, the expression of Caspase-3 was significantly reduced compared with the overload training group (P<0.05), while Caspase-9 expression showed a slight decline (P>0.05).</p><p><b>CONCLUSION</b>Tet preconditioning increased the expression of Bcl-2 and reduced the expression of Caspase-3, thereby attenuating overload training-induced myocardial apoptosis, protecting against overload training-induced myocardial injury, and reducing damage to the myocardium due to overload training.</p>
Subject(s)
Animals , Male , Apoptosis , Caspase 3 , Metabolism , Caspase 9 , Metabolism , Immunohistochemistry , Myocardium , Pathology , Pyrazines , Pharmacology , Rats, Sprague-Dawley , bcl-2-Associated X Protein , MetabolismABSTRACT
The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phosphorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investigated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion (P<0.05, P<0.01). The Akt activities reached the peak at 15 min after reperfusion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced (P<0.01) in tacrolimus postconditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus post-conditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.
Subject(s)
Animals , Male , Rats , Apoptosis , Immunosuppressive Agents , Pharmacology , Therapeutic Uses , Phosphorylation , Protein Serine-Threonine Kinases , Genetics , Metabolism , RNA, Messenger , Genetics , Metabolism , Rats, Sprague-Dawley , Reperfusion Injury , Drug Therapy , Metabolism , Spinal Cord , Metabolism , Pathology , Spinal Cord Ischemia , Drug Therapy , Metabolism , Tacrolimus , Pharmacology , Therapeutic Uses , Up-RegulationABSTRACT
The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phosphorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investigated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion (P<0.05, P<0.01). The Akt activities reached the peak at 15 min after reperfusion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced (P<0.01) in tacrolimus postconditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus post-conditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.
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@#ObjectiveTo research the protective mechanism of acupoint iontophoresis to the heart function.Methods46 SD rats were randomly divided into 5 groups. The methods of histology, transmission electron microscope and radioimmunoassay were used respectively to observe the influence of acupoint iontophoresis on rats' heart ultrastructure.ResultsAcupoint iontophoresis could prolong rats' exertion period, protect ultrastructure of heart and prevent it from abnormal accretion. Over training would cause unbalance secreting between endothelin (ET) and calcitoningene related peptide (CGRP), while acupoint iontophoresis could improve such situation.ConclusionThe rise of exercise induced fatigue is related to many factors; acupoint iontophoresis can protect cardiac muscle, improve heart function and prevent it from exercise induced fatigue via several ways.
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@#Objective To observe effects of acupoint transcutaneus electrical nerve stimulation on endurance training of rats.Methods Rats were put in swimming groove, closed glass bottle and on movable platform, then examined exhausting time, enduring lack of oxygen time, movable platform fatigue time and avoirdupois change.Results Exhausting time, movable platform fatigue time, and enduring lack of oxygen time of experimental rats were increased (P <0.01); All of post experiment rats' avoirdupois rose obviously, but experimental group enhanced least.Conclusion The acupoint transcutaneus electrical nerve stimulation has integrated acupuncture with physical therapy and has features of safety, convenience, practicality and efficiency.