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BACKGROUND:Over-expression of serum interleukin-6 and interleukin-8 may be involved in tourniquet-induced limb ischemia-reperfusion injury to the lung ventilation function. OBJECTIVE:To evaluate the tourniquet effect on serum interleukin-6 and interleukin-8 levels of the rat limb within the safety time limit. METHODS: Sixty rats were randomly divided into control and experimental groups, 30 rats in each group. Rats in the control group had no ischemic preconditioning and were directly subjected to stop bleeding for 2, 3, 4 hours; rats in the experimental group were subjected to ischemic preconditioning (short-time hemostasis for several times within 1 day before ischemia-reperfusion injury), and then underwent 2-, 3-, 4-hour hemostasis at the 2nd day. At 1, 3, 7, 14 days after the recovery of limb blood flow, blood samples were extracted to detect serum interleukin-6 and interleukin-8 levels using ELISA method. RESULTS AND CONCLUSION:The levels of interleukin-6 interleukin-8 showed an increasing and decreasing trend in the two groups, which both reached the peak at the 3rd day (P 0.05), and at 3, 7, 14 days, the level of interleukin-8 in the rats undergoing 4-hour hemostasis was significantly higher than that in the control group (P< 0.05). At 1 and 3 days, the levels of interleukin-6 and interleukin-8 in the experimental group had an increasing trend with the bleeding time and ranked as folows: 2-hour hemostasis < 3-hour hemostasis < 4-hour hemostasis, and there was a significant difference; while in the control group, there was also an increasing trend in the levels of interleukin-6 and interleukin-8, but there was no statistical difference. These findings indicate that the tourniquet preconditioning treatment is preferred at 3 days after limb ischemia-reperfusion injury, when the inflammatory response was the most obvious in rats, and this treatment can dramaticaly reduce inflammatory response. Additionaly, the inflammatory become more obvious with the bleeding time.
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BACKGROUND:Since damage control theory system was founded, this theory in the orthopedics has been applied gradualy, especialy in elderly hip fracture surgery that reduces the negative impacts due to inflammatory responses. OBJECTIVE:To explore whether flurbiprofen axetil can reduce inflammatory responses in rats with hip fractures based on the damage control theory. METHODS: Forty-nine healthy Sprague-Dawley rats weighing 250-300 g were randomly divided into four groups:control group (n=7), immediate internal fixation group (n=14), flurbiprofen axetil group (n=14), damage control group (n=14). Rats in the control group moved freely in the cages. Rats in the other three groups were intraperitonealy injected with composite anesthetics to make unilateral hip fracture models, and then respectively given internal fixation immediately after fracture, flurbiprofen axetil injection and delayed internal fixation, and delayed internal fixation. Levels of serum C-reactive protein, interleukin-6 and tumor necrosis factor-α were determined and analyzed before fixation, immediately after internal fixation and at 4, 8, 12, 24, 48 hours after internal fixation in different groups. RESULTS AND CONCLUSION:Postoperative serum levels of C-reactive protein, interleukin-6, tumor necrosis factor-αwere al increased in different groups. The level of C-reactive protein reached the peak at 24 hours after internal fixation. Flurbiprofen axetil injection had no significant influence on the level of C-reactive protein in rats with delayed internal fixation (P=0.51). Interleukin-6 levels were stil increased at 48 hours after internal fixation, but flurbiprofen axetil reduced the level of interleukin-6 significantly in rats with delayed internal fixation (P < 0.01). The tumor necrosis factor-α level peaked at 4 hours after internal fixation, and flurbiprofen axetil injection could significantly reduce the level of tumor necrosis factor-α in rats with delayed internal fixation (P < 0.01). These findings indicate that flurbiprofen axetil as a new non-steroidal anti-inflammatory drug can reduce the inflammatory response in rats with hip fractures after internal fixation, and also can aleviate the inflammatory response of rats undergoing delayed operation under the guidance of damage control theory.
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BACKGROUND:Bone marrow mesenchymal stem cels are crucial for bone and cartilage development and regeneration at a celular level. Insufficient quantity and functional impairment of bone marrow mesenchymal stem cels is widely considered to be one of osteoarthritis causes. OBJECTIVE: To explore the relationship between the functional status of bone marrow mesenchymal stem cels and disease progression in osteoarthritis patients.METHODS: Thirty patients with osteoarthritis were enroled from July 2013 to October 2014, and divided into control, mild osteoarthritis, and severe osteoarthritis groups, with 10 cases in each group. 5 mL bone marrow from the femur or tibia was extracted from each patient to isolate and culture bone marrow mesenchymal stem cels. Proliferation ability of cels at passage 3 was detected using cel counting kit-8; toluidine blue staining was performed at 14 days after chondrogenic induction; real-time PCR was used to detect the mRNA expression of Aggrecan and Col2A1 in the control group after chondrogenic induction. RESULTS AND CONCLUSION:Afterin vitro culture, bone marrow mesenchymal stem cels grew adherently in polygonal and fusiform shape with multiple processes at uniform size. The cytoplasm contained larger particles and the nuclei were ovoid. Most of cels were in cel division phase. The proliferation ability was strongest in the control group and weakest in the severe osteoarthritis group. Cels from the three groups were al at plateau phase after 1 week culture. At 14 days after chondrogenic induction, the cels were polygonal and quasi-circular, and purple metachromatic granules distributed outside of the cytoplasm. The expression of Aggrecan and Col2A1 in the control group displayed an overexpression trend. These findings indicate that the functional status of bone marrow mesenchymal stem cels from osteoarthritis patients is negatively correlated with the severity of disease, which can influence the disease progression in osteoarthritis patients.
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BACKGROUND:Autophagy can occur in chondrocytes under the low supply of nutrients. Different from necrosis and apoptosis, autophagy can make chondrocytes survive in insufficient supply of nutrients, which may be an important mechanism for the self-protection of chondrocytes. OBJECTIVE: To review the mechanism and effect of autophagy gene to protect the articular cartilage and inhibit osteoarthritis. METHODS:A computer-based search was perform in CNKI, Wanfang, PubMed to retrieve articles addressing autophagy gene and osteoarthritis published from January 2000 to January 2015. The keywords were autophagy, osteoarthritis, articular cartilage, chondrocytes in Chinese and autophagy, osteoarthritis, beclin1, LC3 in English. Totaly 269 articles were initialy searched, and finaly, 38 articles were included in result analysis. RESULTS AND CONCLUSION:Apoptosis of damaged chondrocytes is the main mechanism of articular cartilage degeneration, which can further develop into osteoarthritis. The damage and death of cels is one of the important mechanisms of cartilage degeneration, thus, to prevent damaged chondrocyte apoptosis may help cartilage repair, thus aleviating the progression of osteoarthritis. Autophagy can inhibit damaged chondrocyte apoptosis, which changes the limitations of traditional treatments for osteoarthritis. However, the current research on autophagy genes associated with osteoarthritis is stil at the primary stage, and further studies are needed on how to induce authopagy pathway in the cartilage, how to do the signal transduction and how to have an effect on the survival of chondrocytes.
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BACKGROUND:Autophagy is the celular process of lysosomal pathway processing by endogenous substrates, which exists in the body cels and has been considered as type II programmed cel death. Autophagy may be a protective or balancing mechanism of normal chondrocytes. OBJECTIVE:To discuss the latest research progress in autophagy and cartilage damage aiming to better understanding the role of autophagy in cartilage damage and repair. METHODS:A computer-based search of CNKI, Wanfang database and PubMed database was performed for articles relevant to autophagy and cartilage damage published in recent 20 years with the key words of autophagy, cartilage, chondrocytes, beclin1, LC3 in Chinese and English. RESULTS AND CONCLUSION: Intra-articular chondrocytes can response to the changes in the microenvironment so as to adjust the extracelular matrix metabolism and maintain the biological function of articular cartilage. Hypoxic environment in which chondrocytes eixt is an important factor to causes autophagy. Autophagy is a normal balance or protection mechanism of chondrocytes. Studies on the correlation of autophagy with cartilage damage have made considerable progress in recent years, but stil in its infancy. Atg discovery at the molecular level deepens the understanding of autophagy, but the induction of cartilage autophagy pathway, signal transduction, and their effects on the survival of chondrocytes are not clear yet, which need further studies.
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BACKGROUND:In recent years, many reports have focused on inflammatory cytokines, growth factors and mechanical loads affecting the cartilage and subchondral regeneration, but there is a lack of comprehensive understanding about the mechanism of osteoarthritis. OBJECTIVE: To explore the correlation between function status of bone marrow mesenchymal stem cels and disease progression in patients with osteoarthritis. METHODS:Femoral bone marrow was extracted from patients with femoral neck fractures (control group), mild (mild group) and severe (severe group) osteoarthritis to isolate and culture bone marrow mesenchymal stem cels. Cel counting kit-8 was used to detect the proliferative ability of bone marrow mesenchymal stem cels from different patient groups, and passage 3 bone marrow mesenchymal stem cels were subject to 2-week chondrogenic induction folowed by toluidine blue staining. RESULTS AND CONCLUSION: Bone marrow mesenchymal stem cels were isolated and cultured from the femoral bone marrow of different groups. The proliferative ability of cels in the control group was significantly higher than that in the mild and severe groups. After chondrogenic induction, bone marrow mesenchymal stem cels varied obviously in the morphology that was from fusiform to qusi-circular or polygon, the percentage of nucleoplasm became smaler, and cels were positive for toluidine blue staining. The number of chondrocytes generated in the severe group was less than that in the control group, but there was no great difference in cel morphology. These findings indicate that the occurrence of osteoarthritis is negatively correlated with the functional status of autologous bone marrow mesenchymal stem cels.