Ferroptosis is a necrotic form of regulated cell death that was associated with lipid peroxidation and free iron‐mediated Fenton reactions. It has been reported that iron deficiency had been ...implicated in the pathogenesis of intervertebral disc degeneration (IVDD) by activating apoptosis. However, the role of ferroptosis in the process of IVDD has not been illuminated. Here, we demonstrate the involvement of ferroptosis in IVDD pathogenesis. Our in vitro models show the changes in protein levels of ferroptosis marker and enhanced lipid peroxidation level during oxidative stress. Safranin O staining, hematoxylin‐eosin staining, and immunohistochemical were used to assess the IVDD after 8 weeks of surgical procedure in vivo. Treatment with ferrostatin‐1, deferoxamine, and RSL3 demonstrate the role of ferroptosis in tert‐butyl hydroperoxide (TBHP)‐treated annulus fibrosus cells (AFCs) and nucleus pulposus cells (NPCs). Ferritinophagy, nuclear receptor coactivator 4 (NCOA4)‐mediated ferritin selective autophagy, is originated during the process of ferroptosis in response to TBHP treatment. Knockdown and overexpression NCOA4 further prove TBHP may induce ferroptosis of AFCs and NPCs in an autophagy‐dependent way. These findings support a role for oxidative stress‐induced ferroptosis in the pathogenesis of IVDD.
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Ferroptosis is a necrotic form of regulated cell death that was associated with lipid peroxidation and free iron‐mediated Fenton reactions. It has been reported that iron deficiency had been implicated in the pathogenesis of intervertebral disc degeneration (IVDD) by activating apoptosis. However, the role of ferroptosis in the process of IVDD has not been illuminated. Here, we demonstrate the involvement of ferroptosis in IVDD pathogenesis.
High dose and long‐term steroid treatment can alter antioxidative ability and decrease the viability and function of osteoblasts, leading to osteoporosis and osteonecrosis. Ferroptosis, a new type of ...cell death characterized by excessive lipid peroxidation due to the downregulation of GPX4 and system Xc−, is involved in glucocorticoid‐induced osteoporosis. Endothelial cell‐secreted exosomes (EC‐Exos) are important mediators of cell‐to‐cell communication and are involved in many physiological and pathological processes. However, the effect of EC‐Exos on osteoblasts exposed to glucocorticoids has not been reported. Here, we explored the role of EC‐Exos in glucocorticoid‐induced osteoporosis. In vivo and in vitro experiments indicated that EC‐Exos reversed the glucocorticoid‐induced osteogenic inhibition of osteoblasts by inhibiting ferritinophagy‐dependent ferroptosis.
Here, we explored the role of EC‐Exos in glucocorticoid‐induced osteoporosis. In vivo and in vitro experiments indicated that EC‐Exos reversed the glucocorticoid‐induced osteogenic inhibition of osteoblasts by inhibiting ferritinophagy‐dependent ferroptosis.
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The work investigated the potential application of Mg-laden biochar prepared from Mg-enriched bamboo to remove and recover phosphate from water. The Mg-laden biochar samples were ...synthesized at 400 °C, 500 °C and 600 °C. With the increasing synthesized temperature, the production rate of adsorbent decreased but the Mg content and specific surface area increased. Factors on phosphate adsorption including kinetic, isotherm, pH, dosage were examined through batch experiments. The maximum phosphate adsorption amount was 344, 357 and 370 mg/g for biochar-Mg-400, biochar-Mg-500 and biochar-Mg-600, respectively. The effect of phosphate adsorption on Mg-laden biochar samples was also investigated by fixed-bed column experiments, and the maximum adsorption amount calculated by Thomas model was 60.7, 61.2 and 62.2 mg/g, respectively. The adsorbed phosphate could be successfully desorbed by 3 M NaOH solution and the regenerated Mg-laden biochar samples could be reused at least 5 times for phosphate adsorption. The bioavailability of postsorption biochar was proved very well through the Mehlich 3 method. Phosphate adsorption characteristic and FTIR analysis indicated that the adsorption was mainly controlled by two mechanisms: ligand exchange and electrostatic attraction.
The main pathological mechanism of intervertebral disc degeneration (IVDD) is the programmed apoptosis of nucleus pulposus (NP) cells. Oxidative stress is a significant cause of IVDD. Whether ...mitophagy is induced by strong oxidative stress in IVDD remains to be determined. This study aimed to investigate the relationship between oxidative stress and mitophagy and to better understand the mechanism of IVDD in vivo and in vitro. To this end, we obtained primary NP cells from the human NP and subsequently exposed them to TBHP. We observed that oxidative stress induced mitophagy to cause apoptosis in NP cells, and we suppressed mitophagy and found that NP cells were protected against apoptosis. Interestingly, TBHP resulted in mitophagy through the inhibition of the HIF-1α/NDUFA4L2 pathway. Therefore, the upregulation of mitochondrial NDUFA4L2 restricted mitophagy induced by oxidative stress. Furthermore, the expression levels of HIF-1α and NDUFA4L2 were decreased in human IVDD. In conclusion, these results demonstrated that the upregulation of NDUFA4L2 ameliorated the apoptosis of NP cells by repressing excessive mitophagy, which ultimately alleviated IVDD. These findings show for the first time that NDUFA4L2 and mitophagy may be potential therapeutic targets for IVDD.
Previous work reveals that the magnetically coupled resonant (MCR) wireless power transfer (WPT) technology is efficient and practical for mid-range wireless energy transmission, able to handle ...nontrivial amount of power. Due to the variable coupling coefficient under lateral misalignment and angular misalignment between transmitting coils and receiving coils, the output power and transmission efficiency will fluctuate, leading to instability of the system. This paper presented an equivalent analytical model for the MCR WPT system to incorporate spatial misalignments. The mutual inductance formulas were derived when receiving coils are laterally, angularly or generally misaligned from transmitting coils. The relationship among the output power, transmission efficiency, the mutual inductance, and load resistance were analyzed in detail. For the design of the MCR WPT system, it is necessary to seek optimal transmission performance under different applications. To achieve maximum output power and high stability of power transfer in a specific misalignments range, a normalization method based on the obtained analytical model was introduced, providing critical insight into the optimal design of coils. Relative design considerations and optimization procedures were further stated. Experiments had also been carried out to evaluate the accuracy of theoretical analysis and confirm the validity of the proposed optimization method.
β-Conglycinin has been identified as one of the major feed allergens. However, studies of β-conglycinin on fish are scarce. This study investigated the effects of β-conglycinin on the growth, ...digestive and absorptive ability, inflammatory response, oxidative status and gene expression of juvenile Jian carp (Cyprinus carpio var. Jian) in vivo and their enterocytes in vitro. The results indicated that the specific growth rate (SGR), feed intake, and feed efficiency were reduced by β-conglycinin. In addition, activities of trypsin, chymotrypsin, lipase, creatine kinase, Na(+),K(+)-ATPase and alkaline phosphatase in the intestine showed similar tendencies. The protein content of the hepatopancreas and intestines, and the weight and length of the intestines were all reduced by β-conglycinin. β-Conglycinin increased lipid and protein oxidation in the detected tissues and cells. However, β-conglycinin decreased superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and glutathione (GSH) content in the intestine and enterocytes. Similar antioxidant activity in the hepatopancreas was observed, except for GST. The expression of target of rapamycin (TOR) gene was reduced by β-conglycinin. Furthermore, mRNA levels of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β) genes were increased by β-conglycinin. However, β-conglycinin increased CuZnSOD, MnSOD, CAT, and GPx1b gene expression. In conclusion, this study indicates that β-conglycinin induces inflammation and oxidation, and causes dysfunction of intestinal digestion and absorption in fish, and finally reduces fish growth. The results of this study provide some information to the mechanism of β-conglycinin-induced negative effects.
Medium‐entropy (Ti,Zr,Hf)C ceramics were prepared by hot pressing a dual‐phase medium‐entropy carbide powder with low oxygen content (0.45 wt%). The results demonstrate that the medium‐entropy ...(Ti,Zr,Hf)C ceramics sintered at 2100°C had a relative density of 99.2% and an average grain size of 1.9 ± 0.6 μm. The flexural strength of (Ti,Zr,Hf)C carbide ceramics at room temperature was 579 ± 62 MPa. With an increase in temperature to 1600°C, the flexural strength showed an increase up to 619 ± 57 MPa, and had no significant degradation even up to 1800°C. The high‐temperature flexural strengths of (Ti,Zr,Hf)C were obviously higher than those of the monocarbide ceramics (TiC, ZrC, and HfC). The primary strengthening mechanism in (Ti,Zr,Hf)C could be attributed to the high lattice parameter mismatch effects between TiC and ZrC, which not only inhibited the fast grain coarsening of (Ti,Zr,Hf)C ceramics, but also increased the grain‐boundary strength of the obtained ceramics.
Copper (Cu) is a common heavy metal pollutant in aquatic environments that originates from natural as well as anthropogenic sources. The present study investigated whether Cu causes oxidative damage ...and induces changes in the expression of genes that encode tight junction (TJ) proteins, cytokines and antioxidant-related genes in the intestine of the grass carp (Ctenopharyngodon idella). We demonstrated that Cu decreases the survival rate of fish and increases oxidative damage as measured by increases in malondialdehyde and protein carbonyl contents. Cu exposure significantly decreased the expression of genes that encode the tight junction proteins, namely, claudin (CLDN)-c, -3 and -15 as well as occludin and zonula occludens-1, in the intestine of fish. In addition, Cu exposure increases the mRNA levels of the pro-inflammatory cytokines, specifically, IL-8, TNF-α and its related signalling factor (nuclear factor kappa B, NF-κB), which was partly correlated to the decreased mRNA levels of NF-κB inhibitor protein (IκB). These changes were associated with Cu-induced oxidative stress detected by corresponding decreases in glutathione (GSH) content, as well as decreases in the copper, zinc-superoxide dismutase (SOD1) and glutathione peroxidase (GPx) activities and mRNA levels, which were associated with the down-regulated antioxidant signalling factor NF-E2-related factor-2 (Nrf2) mRNA levels, and the Kelch-like-ECH-associated protein1 (Keap1) mRNA levels in the intestine of fish. Histidine supplementation in diets (3.7 up to 12.2 g/kg) blocked Cu-induced changes. These results indicated that Cu-induced decreases in intestinal TJ proteins and cytokine mRNA levels might be partially mediated by oxidative stress and are prevented by histidine supplementation in fish diet.
Background/Aims: Apoptosis and autophagy are two patterns of programmed cell death which play important roles in the intervertebral disc degeneration. Oxidative stress is an important factor for the ...induction of programmed cell death. However, the cellular reactions linking autophagy to apoptosis of disc cells under oxidative stress have never been described. This study investigated the responses of autophagy and apoptosis and their interactions in the nucleus pulposus cells (NP cells) under oxidative stress, with the aim to better understand the mechanism of disc degeneration. Methods: NP cells isolated from rat lumbar discs were subjected to different concentrations of H2O2 for various time periods. Cell viability was determined by CCK-8 assay, and their apoptosis and autophagy responses were evaluated by fluorescent analysis, flow cytometry and western blotting, et al. The interactions of autophagy and apoptosis and the possible signaling pathways were also investigated by using autophagy modulators. Results: H2O2 increased the lysosomal membrane permeability in the NP cells and induced apoptosis through the mitochondrial pathway subsequently. Meanwhile, H2O2 stimulated an early autophagy response through the ERK/m-TOR signaling pathway. Autophagy inhibition significantly decreased the apoptosis incidence in the cells insulted by H2O2. Conclusion: These results suggested that controlling the autophagy response in the NP cells under oxidative stress should be beneficial for the survival of the cells and probably delay the process of disc degeneration.
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