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BACKGROUND: Oxidative stress plays an important role in femoral head necrosis. Platelet-rich plasma (PRP) contains growth factors that can accelerate fracture healing. PRP combined with core decompression can promote recovery from non-traumatic femoral head necrosis. OBJECTIVE: To investigate whether PRP combined with core decompression can inhibit oxidative stress in steroid-induced avascular necrosis of the femoral head model via Keap1/Nrf2/HO-1 signaling pathway. METHODS: Forty New Zealand rabbits were randomly divided into normal group, model group, control group and PRP group, with 10 rabbits in each group. In the model and PRP groups, a model of steroid-induced femoral head necrosis was established in a sterile environment. At 4 weeks after operation, the rabbits in the PRP group were injected with 0.4 mL of 3% PRP after core decompression. The control group received core decompression treatment, and the control and model groups were raised normally. After 14 weeks, the experimental animals were sacrificed. Hematoxylin-eosin staining was used to observe the pathological changes of bone marrow cavity and the vacancy rate of bone lacunae in the femoral head of each group. Total antioxidant capacity, superoxide dismutase, glutathione peroxidase, reduced glutathione, and malondialdehyde were detected. TUNEL was used to detect bone cell apoptosis in the femoral head. Immunofluorescence staining was used to determine the distribution of Keap1 and Nrf2. Western blot was used to measure Keap1, Nrf2, and H0-1 protein expression in the femoral head. Approval was obtained from the Animal Ethics Committee of the Affiliated Hospital of Qinghai University, approval No. qhdx-201908374. RESULTS AND CONCLUSION: (1) Compared with the normal group, the trabecular bone in model group was thinned with structure disorder. Compared with the model group, the trabecular bone structure in control group was restored, and the number of vacant bone lacunae was reduced (P < 0.05). Compared with the control group, the animals treated with PRP combined with core decompression were further improved, the trabecular bone structure was further improved, and the number of vacant bone lacunae was further reduced (P < 0.05). Whereas there was no significant difference between the PRP group and normal group (P > 0.05). (2) The total antioxidant capacity and serum levels of superoxide dismutase, glutathione peroxidase, and reduced glutathione in the model group were significantly lower than those in normal animals (P < 0.05), while the MDA concentration was significantly higher than that in the normal group (P < 0.05). These oxidative stress indexes were slightly improved in the control group compared with the model group (P > 0.05), while these indexes were significantly improved in the PRP group than the model and control groups (P < 0.05). (3) The expression of Kesp1 in the model group was significantly lower than that of the normal group (P < 0.05), and the expression of Nrf2 and HQ-1 protein was significantly higher than that of the normal group (P < 0.05). The expression of Keap1 in the PRP group was lower than that of the model and control groups (P < 0.05), and the expression of Nrf2 and HQ-1 was significantly higher than that of the model and control groups (P < 0.05). Therefore, PRP can effectively inhibit oxidative stress in the process of steroid-induced femoral head necrosis, which may be caused by activating the Keap1/Nrf2/HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]

Doxorubicin (DOX) is one of the most effective chemotherapeutic drugs; however, the incidence of cardiotoxicity compromises its therapeutic index. Oxidative stress and apoptosis are believed to be involved in DOX-induced cardiotoxicity. Chitosan oligosaccharides (COS), the enzymatic hydrolysates of chitosan, have been reported to possess diverse biological activities including antioxidant and anti-apoptotic properties. The objective of the present study was to investigate the potential role of COS against DOX-induced cardiotoxicity, and the effects of COS on apoptosis and oxidative stress in rats and H9C2 cells. Furthermore, we also shed light on the involved pathways during the whole process. For this purpose, first, we demonstrated that COS exhibited a significant protective effect on cardiac tissue by not only inducing a decrease in body and heart growth but also ameliorated oxidative damage and ECG alterations in DOX-treated rats. Second, we found that COS reversed the decrease of cell viability induced by DOX, reduced the intracellular reactive oxygen species (ROS), increased the mitochondrial membrane potential (MMP) and Bcl-2/Bax ratio. COS treatment also results in reduced caspase-3 and caspase-9 expressions, and an increase in the phosphorylation of MAPKs (mitogen-activated protein kinases) in DOX-exposed H9C2 cells. Additionally, cellular homeostasis was re-established via stabilization of MAPK mediated nuclear factor erythroid 2-related factor 2/antioxidant-response element (Nrf2/ARE) signaling and transcription of downstream cytoprotective genes. In summary, these findings suggest that COS could be a potential candidate for the prevention and treatment of DOX-induced cardiotoxicity. • COS significantly protects against doxorubicin-induced cardiotoxicity in vivo. • COS prevents oxidative stress and cardiac apoptosis induced by doxorubicin. • COS prevents doxorubicin cardiotoxicity via p38, JNK MAPK-mediated Nrf2/ARE pathway. [ABSTRACT FROM AUTHOR]

A systematic study was made to determine the effects of aluminizing temperature and time on the growth of the Ni 2 Al 3 coating on the electrodeposited nanocrystalline (NC) Ni with and without La 2 O 3 /CeO 2 nanoparticles by the pack aluminizing process at 550 °C/600 °C. The results show that the growth of Ni 2 Al 3 coating obeyed the parabolic law after a delay time (t 0), which decreased with increment of aluminizing temperature. The addition of La 2 O 3 /CeO 2 nanoparticles significantly refined the grain of aluminide. The La 2 O 3 /CeO 2 -dispersed Ni 2 Al 3 coatings exhibit a lower oxidation rate than the La 2 O 3 /CeO 2 -free one in air at 900 °C, because of various effects of La 2 O 3 /CeO 2 on the oxidation including the grain refinement effect of the aluminide, the "reactive element effect" (REE) and the epitaxial template effect of La 2 O 3 to promote the growth of α-Al 2 O 3. Furthermore, the accumulation of La 2 O 3 particles at the degradation front slightly inhibited the interdiffusion between the aluminide and Ni; while the formation of a CeO 2 -rich layer between aluminide and Ni–CeO 2 film significantly mitigated the degradation of aluminide coatings. • The growth of Ni 2 Al 3 coating on the electrodeposited Ni at 550℃ and 600℃ obeyed the parabolic law. • The La 2 O 3 /CeO 2 -dispersed Ni 2 Al 3 coatings exhibited improved oxidation resistance compared to the La 2 O 3 /CeO 2 -free one. • The La 2 O 3 dispersion promoted the growth of α-alumina, while the CeO 2 dispersion suppressed the growth of θ-Al 2 O 3. • The accumulation of La 2 O 3 particles at the degradation front slightly inhibited the interdiffusion between aluminide and Ni. • The formation of a CeO 2 -rich layer between aluminide and Ni-CeO 2 film significantly mitigated the degradation of aluminide. [ABSTRACT FROM AUTHOR]

A series of novel β-elemene dimer derivatives were synthesized and evaluated for their antioxidant activities. The results indicated that most of the target compounds showed more potent cytoprotective effects than positive control vitamin E. In particular, dimer D5 exhibited the strongest antioxidant activity, which was significantly superior to the active compound D1 obtained in our previous study. Besides, D5 did not produce obvious cytotoxicity in normal human umbilical vein endothelial cells (HUVECs) and increased the viability of HUVECs injured by H 2 O 2 in a concentration-dependent manner. Further studies suggested that the cytoprotective action of D5 might be mediated, at least in part, by increasing the intracellular superoxide dismutase activity and nitric oxide secretion as well as decreasing the intracellular malonyldialdehyde content and lactate dehydrogenase release. Furthermore, D5 observably inhibited ROS generation and prevented H 2 O 2 -induced apoptosis in HUVECs possibly via inhibiting the activation of the MAPK signaling pathway.