Background: Osteoblast apoptosis induced by oxidative stress plays a crucial role in the development and progression of osteoporosis. Curcumin, a natural antioxidant isolated from Curcuma longa, has highly protective effects against osteoporosis. However, the effects of curcumin on oxidative stressinduced osteoblast apoptosis remain unclear. This study aimed to explore the effect of curcumin on hydrogen peroxide (H 2 O 2 ) induced osteoblast apoptosis and the underlying mechanisms. Methods: An osteoblastic cell line (Saos-2) was exposed to various concentrations of H 2 O 2 with or without curcumin treatment. Cell viability was evaluated by MTT assays. The apoptosis rate was analyzed by flow cytometry and TUNEL assays. Mitochondrial ROS and membrane potential were determined using a fluorescence microscope. Mitochondrial respiratory enzyme activity was measured using a spectrophotometer. Protein levels were detected by western blotting. Results: Curcumin was cytoprotective because it greatly improved the viability of Saos-2 cells exposed to H 2 O 2 and attenuated H 2 O 2 -induced apoptosis. Curcumin treatment also preserved the mitochondrial redox potential, decreased the mitochondrial oxidative status, and improved the mitochondrial membrane potential and functions. Furthermore, curcumin treatment markedly increased levels of phosphorylated protein kinase B (Akt) and phosphorylated glycogen synthase kinase-3β (GSK3β). Conclusion: Curcumin administration ameliorates oxidative stress-induced apoptosis in osteoblasts by preserving mitochondrial functions and activation of Akt-GSK3β signaling. These data provide experimental evidence supporting the clinical use of curcumin for prevention or treatment of osteoporosis.P. Dai and Y. Mao contributed equally to this work.
Background: Dunaliella salina is a good model organism for studying salt stress. In order to have a global understanding of the expression profiles of Dunaliella salina in response to hypersaline stress, we performed quantitative transcriptomic analysis of Dunaliella salina under hypersaline stress (2.5 M NaCl) of different time duration by the second and third generation sequencing method. Results: Functional enrichment of the up-regulated genes was used to analyze the expression profiles. The enrichment of photosynthesis was observed, accompanied by enrichments of carbon fixation, pigment biosynthetic process and heme biosynthetic process, which also imply the enhancement of photosynthesis. Genes responsible for starch hydrolysis and glycerol synthesis were significantly up-regulated. The enrichment of biosynthesis of unsaturated fatty acids implies the plasma membrane undergoes changes in desaturation pattern. The enrichment of endocytosis implies the degradation of plasma membrane and might help the synthesis of new glycerophospholipid with unsaturated fatty acids. Co-enrichments of protein synthesis and degradation imply a higher protein turnover rate. The enrichments of spliceosome and protein processing in endoplasmic reticulum imply the enhancement of regulations at post-transcriptional and post-translational level. No up-regulation of any Na + or Cl − channels or transporters was detected, which implies that the extra exclusion of the ions by membrane transporters is possibly not needed. Voltage gated Na + and Cl − channels, mechanosensitive ion channel are possible signal receptors of salt stress, and Ca 2+ and MAP kinase pathways might play a role in signal transduction. Conclusion: At global transcriptomic level, the response of Dunaliella salina to hypersaline stress is a systematic work, possibly involving enhancements of photosynthesis, carbon fixation, and heme biosynthetic process, acceleration of protein turnover, spliceosome, protein processing in endoplasmic reticulum, and endocytosis, as well as degradation of starch, synthesis of glycerol, membrane lipid desaturation. Altogether, the changes of these biological processes occurred at trancriptomic level will help understand how a new intracellular balance achieved in Dunaliella salina to adapt to hypersaline environment, which are worth being confirmed at the physiological levels.
Cervical squamous cell carcinoma (CSCC) is a type of female cancer that affects millions of families worldwide. Human papillomavirus (HPV) infection is the main reason for CSCC formation, and squamous intraepithelial lesions (SILs) induced by high-risk HPV (HR-HPV) infection are considered precancerous lesions. A previous study reported that HPV-infected cancer cells were able to counteract lipid peroxidation for survival. Recent research has reported that ferroptosis acts in an iron-dependent lipid peroxidation manner to kill cancer cells, and it is proposed as a new approach for female cancer therapy. Here, we investigated the role of ferroptosis throughout SIL development into CSCC. We found that ferroptosis occurred in SIL, but anti-ferroptosis emerged in CSCC. Our data further indicated that an antiferroptotic effect was formed in response to persistent ferroptosis and then promoted oncogenesis. Altogether, we provide novel insight into ferroptosis in cervical SIL development and suggest a potential therapeutic target for the treatment of CSCC.
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