Résumé
BACKGROUND: Due to the close relationship between the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway and the physiological metabolism of bone tissue, human chitinase protein 40 (YKL-40) can regulate the PI3K/Akt signaling pathway related to breast cancer pathogenesis. Therefore, it is speculated that YKL-40 may regulate apoptosis in knee osteoarthritis (KOA) chondrocytes through the PI3K/Akt signaling pathway. OBJECTIVE: To study the mechanism by which YKL-40 regulates apoptosis in rabbit KOA chondrocyte s through the PI3K/Akt signaling pathway. METHODS: (1) New Zealand white rabbits were randomized into two groups. An animal model of KOA was made using anterior cruciate ligament dissection in the model group, whereas the right posterior knee joint capsule was cut but not dissected in the control group. Chondrocytes were extracted from the rabbits at 6 weeks after modeling. Hematoxylin-eosin staining and Mankin histological scoring of the cartilage tissue were performed, whereas immunohistochemical staining was used to detect type II collagen expression in chondrocytes. (2) The second-generation chondrocytes in the control group were used as normal control group, and those in the model group were further divided into four groups, followed by culture with high glucose DMEM medium containing 10% fetal bovine serum in KOA model group, 100 μg/L YKL-40 in KOA + YKL group, 50 µmol/L LY294002 in KOA + LY group, and 50 µmol/L LY294002 + 100 μg/L YKL-40 in KOA + YKL + LY group. The expression levels of collagen type II, matrix metalloproteinase 13, Akt, p-Akt, P53, Bcl-2 proteins in chondrocytes were detected by western blot. RESULTS AND CONCLUSION: Hematoxylin-eosin staining, Mankin histological score, and collagen type II immunohistochemical staining confirmed the successful construction of KOA animal model and successful chondrocyte culture. Compared with the normal control group, the collagen type II, Bcl-2, p-Akt protein expression levels in chondrocytes were significantly reduced in the KOA model group (P 0.05). However, there were significant differences between the KOA + YKL group and the KOA + LY group (P 0.05). To conclude, YKL-40 can inhibit the apoptosis of KOA chondrocytes, accelerate the repair of KOA cartilage damage and delay the degeneration of cartilage by activating the PI3K/Akt signaling pathway. Therefore, YKL-40 can be used as a new target for clinical treatment of KOA.
Résumé
Objective To investigate the effects of goal‐directed volume therapy (GDVT )on the intracranial pressure(ICP) and the balance of cerebral oxygen consumption and supply in selective neurosurgery. Methods Twenty‐four patients sched‐uled for intracranial tumor resection were randomly divided into 2 groups:conventional fluid management group (group C ,n=12) and GDVT group(group G ,n=12). Patients in group C received introperative fluid transfusion according to classical fluid management strategies while those in group G received GDT according to stroke volume variation (SVV) ,guided by Flotrac‐Vigileo system.Mean arterial pressure(MAP) ,heart rate(HR) ,cardiac index(CI) ,ICP ,SVV and jugular bulb oxygen saturation (SjvO2 )were recorded before the anesthesia induction(T1 ) ,at the moment of intubation(T2 ) ,at the moment of opening the hard meninges(T3),1hafteropeningthehardmeninges(T4),andattheendofthesurgery(T5).Thecerebraloxygenextractionra‐tio(CERO2 )was calculated. The duration of surgery ,crystalloid volume ,colloid volume ,blood transfusion volume ,urinary output and bleeding volume were recorded as well.Results The colloid transfusion volume ,the total fluid transfusion volume and uri‐nary output were significantly increased in group G when compared with those in group C (P0.05).Conclusion Goal‐directed fluid therapy optimizes the cardiac preload without increasing the ICP in selective neurosurgery ,and it also improves the balance of cerebral oxygen con‐sumption and supply.