• Journal of Acupuncture Research
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• v.19 no.2
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• pp.51-64
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• 2002

We have compared(using the same series of experimental tissue samples) the levels of proteolytic enzyme activities and free radical-induced protein damage in synovial fluid from RA and CPH cases. Many protease types showed significantly increased (typically by a factor of approximately 2-3-fold) activity in RA, compared to normal rats. However, CPH significantly reduced the cytoplasmic enzyme activities of arginyl aminopeptidase, leucyl aminopeptidase, pyroglutamyl aminopeptidase, tripeptidyl aminopeptidase, and proline endopeptidase to almost about 1/10 each. For the Iysosomal proteases, synovial fluid samples from RA rats, CPH significantly reduced the enzyme activities of cathepsin B, dipeptidyl aminopeptidase I and dipeptidyl aminopeptidase II. In extracellular matrix degrading(collagenase, tissue elastase) and leukocyte as sociated proteases (leukocyte elastase, cathepsin G), CPH decreased these enzyme activities of collagenase, tissue elastase and leukocyte associated elastase in RA. In cytoplasmic and lysosomal protease activities in plasma from RA. CPH and normal plasma samples were not significantly different, suggesting that altered activity of plasma proteases (particularly those enzymes putatively involved in the immune response) is not a contributory factor in the pathogenesis of RA. In addition, the level of free radical induced damage to synovial fluid proteins was approximately twice that in RA, compared with CPH. CPH significantly decreased the level of ROS induced oxidative damage to synovial fluid proteins (quantified as protein carbonyl derivative). Therefore we conclude that both proteolytic enzymes and free radicals are likely to be of equal potential importance as damaging agents in the pathogenesis of inflammatory joint disease, and that the design of novel therapeutic strategies for patients with the latter disorder should include both protease inhibitory and free radical scavenging elements. In addition, the protease inhibitory element should be designed to inhibit the action of a broad range of protease mechanistic types (i.e. cysteine-, metallo- and serine- proteinases and peptidases). However, increased protein damage induced by ROS could not be rationalised in terms of compromised antioxidant total capacity, since the latter was not significantly altered in RA synovial fluid or plasma compared with CPH.

• Korean Journal of Food Science and Technology
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• v.40 no.6
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• pp.674-679
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• 2008

Scutellaria radix (SR) has been utilized as a traditional medicine for a variety of diseases including Rheumatoid arthritis and its major flavonoids - baicalein, baicalin, and wogonin - have been reported to exert beneficial health effects, including anti-bacterial, anti-viral, anti-inflammatory, and free-radical scavenging. However, the mechanisms underlying this effect remain poorly understood. The principal objective of this study was to determine the effect of SR on osteoblast and osteoclast cells. SR extract was prepared using 70% ethanol solvent. Osteoblastic MC3T3-E1 cells and osteoclast precursor Raw 264.7 macrophage cells were utilized. SR extract increased MC3T3-E1 cell proliferation and stimulated alkaline phosphatase activity dose-dependently, 152.0% of the control at concentration $1{\mu}g/mL$. Additionally, SR extract ($1{\mu}g/mL$) stimulated Bone nodule formation activity in MC3T3-E1 cells, approximately 223.3% of the control, 20 days after the exposure. In addition, SR extract significantly reduced the number of tartrate-resistant acid phosphatase-positive (TRAP+) multinucleated cells from Raw 264.7 cells. In conclusion, SR extract stimulates the proliferation and bioactivities of boneforming osteoblasts, and inhibits the activities of bone-resorbing osteoclasts to a certain degree.

• Journal of Periodontal and Implant Science
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• v.26 no.2
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• pp.448-468
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• 1996

To maintain its functional integrity, bone is continuously remodelled by a process involving resorption by osteoeclasts and formation by osteoblasts, In order to respond to changes in the physical environment or to trauma with the relevant action, this process is strictly regulated by locally synthesized or systemic fators, Prostaglandin $E_2(PGE_2$) is perhaps one of the best studied factors, having been known to affect bone cell function for several decades.$PGE_2$ has both anabolic and catabolic activities. Excess of $PGE_2$ has been implicated in a number of pathological states associated with bone loss in a number of chronic inflammatory conditions such as periodontal disease and rheumatoid arthritis. $PGE_2$ and other arachidonic acid metabolites have been shown to be potent stimulators of osteoclastic bone resorption in organ culture. The anabolic effects of $PGE_2$ were first noticed when an increase in periosteal woven bone formation was seen after the infusion of $PGE_2$ into infants in order to prevent closure of the ductus arteriosus. The cellular basis for the catabolic actions of $PGE_2$ has been well characterized. $PGE_2$increases osteoclast recruitment in bone marrow cell cultures. Also $PGE_2$ has a direct action on osteoclast serving to inhibit activity and can also indirectly activate osteoclast via other cells in the vicinity, presumably osteoblast. The cellular mechanisms for the anabolic actions of $PGE_2$ are not nearly so well understood. The purpose of this paper was to study the effects of $PGE_2$ and dibutyl(DB)cAMP on osteoblastic clone MC3T3El cells and on the generation of osteoclasts from their precursor cells. The effect of $PGE_2$ and DBcAMP on the induction of alkaline phoaphatase(AlP) was investigated in osteoblastic clone MC3T3El cells cultured in medium containing 0.4% fetal bovine serum. $PGE_2$ and DBcAMP stimulated ALP activity and MTT assay in the cells in a dose-dependent manner at concentrations of lO-SOOng/ml. Cycloheximide, protein synthesis inhibitor, inhibited the stimulative effect of $PGE_2$ and DBcAMP on ALP activity in the cells. $PGE_2$also increased the intracellular cAMP content in a dose-dependent fashion with a maximal effect at 500ng/ml. The effect of $PGE_2$ on the generation of osteoclasts was investigated in a coculture system of mouse bone marrow cells with primary osteoblastic cells cultured in media containing 10% fetal bovine serum.After cultures, staining for tartrate-resistant acid phosphatase(TRAP)-marker enzyme of osteoclast was performed. The TRAP(+) multinucleated cells(MNCs), which have 3 or more nuclei, were counted. More TRAP(+) MNCs were formed in coculture system than in control group. $PGE_2(10^{-5}10^{-6}M)$ stimulated the formation of osteoclast cells from mouse bone marrow cells in culture. $PGE_2(10^{-6}M)$ stimulated the formation of osteoclast cells from mouse bone marrow cells in coculture of osteoblastic clone MC3T3E1 cells This results suggest that $PGE_2$ stimulates the differentiation of osteoblasts and generation of osteoclast, and are involved in bone formation, as well as in bone resorption.

• Journal of the Korean Orthopaedic Association
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• v.56 no.6
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• pp.504-511
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• 2021

Purpose: This study examined the difference between the drainage volume, blood loss, transfusion rate, volume, and complications with or without an intra-articular (IA) tranexamic acid (TXA) injection among patients who underwent simultaneous bilateral total knee arthroplasty (SBTKA) with bilateral knee joint osteoarthritis, including patients who have contraindications of intravenous administration. Materials and Methods: Among patients who underwent SBTKA from April 2016 to December 2018, 139 patients injected with 3 g of TXA in each side through a drainage tube after joint capsule repair (group T), and 57 patients (group A) who underwent the procedure without TXA between October 2007 and August 2010 were tested. No significant difference in age and sex was observed between the two groups (p=0.572, 0.474). TXA was injected in patients with contraindications of intravenous administrations. Patients who underwent SBTKA with inflammatory arthritis were excluded from this study. The average amount of drainage, blood loss, transfusion rate, volume and daily average transfusion rate, and hemoglobin (Hb) change by the postoperative day were compared. Complications, such as deep vein thrombosis, pulmonary thromboembolism, myocardial infarction, cerebral infarction, and infection, were investigated. Results: The average total blood losses in groups A and T were 2195.32±1175.63 ml and 1145.09±382.95 ml, respectively, and the average total drain volume was 1,178.30±48.59 ml and 774.19±310.06 ml, respectively; both were significantly lower in group T (p=0.002, <0.001). The transfusion rates were 77.2% (44/57) and 0.7% (1/139), which were significantly lower in group T (p<0.001). The total average transfusion volume in groups A and T were 735.44±550.83 ml and 4.60±54.28 ml, respectively, which were significantly lower in group T (p<0.001). Hb tended to increase for three or four days after surgery in group A and group T. Regarding complications, deep vein thrombosis was encountered in two cases (1.4%), and pulmonary thromboembolism was noted in three cases (2.2%) in group T, but there were no cases in group A. No infections, cerebral infarction, or myocardial infarction occurred. Conclusion: In SBTKA, IA injections of TXA reduced the average drain volume, blood loss, transfusion rate, and volume significantly and did not increase the incidence of complications, even in patients with contraindications of intravenous administration.