Osteopontin-induced brown adipogenesis from white preadipocytes through a PI3K-AKT dependent signaling.

Recent studies have shown that OPN (osteopontin) plays critical roles in cell survival, differentiation, bio-mineralization, cancer and cardiovascular remodeling. However, its roles in the differentiation of brown adipocytes and the underlying mechanisms remain unclear. Therefore, the aim of this study was to investigate the roles of OPN in the brown adipogenesis and the underlying mechanisms. It was shown that the OPN successfully induced the differentiation of 3T3-L1 white preadipocytes into the PRDM16(+) (PRD1-BF1-RIZ1 homologous domain containing 16) and UCP-1(+) (uncoupling protein-1) brown adipocytes in a concentration and time-dependent manner. Also, activation of PI3K (phosphatidylinositol 3-kinase)-AKT pathway was required for the OPN-induced brown adipogenesis. The findings suggest OPN plays an important role in promoting the differentiation of the brown adipocytes and might provide a potential novel therapeutic approach for the treatment of obesity and related disorders.

The role of anxiety in the association between nutrition literacy and health-related quality of life among college students.

The health-related quality of life (HRQOL) of college students is not promising and needs to be improved through effective interventions. This study aimed to investigate the associations of nutrition literacy (NL) with HRQOL and anxiety among college students, and to identify the role of anxiety in the relationship between NL and HRQOL. The cross-sectional survey was conducted via the "Wenjuanxing" platform from September to November 2023. The Food and Nutrition Literacy Questionnaire (FNLQ), the Generalized Anxiety Disorder (GAD-7) diagnostic tool and the SF-12 scale were used to assess NL, anxiety, and HRQOL, respectively. Logistic regression models, mediation analysis, additive and multiplicative interaction analyses were used. 2066 college students participated in the analysis. After adjusting for potential confounders, we found that college students with higher NL had higher HRQOL (OR = 2.52, 95% CI: 2.09-3.03, p < 0.001) and a lower risk of anxiety (OR = 0.53, 95% CI: 0.39-0.73, p < 0.001). Additionally, anxious college students had lower HRQOL (OR = 0.16, 95% CI: 0.11-0.24, p < 0.001). Furthermore, mediation analysis confirmed that anxiety was a partial mediator of the relationship between NL and HRQOL (ß = 0.600, 95% CI: 0.406-0.779/0.430-0.818). Significant additive interactions were found between NL and Anxiety (RERI = 6.96, 95% CI: 2.74-11.17; AP = 0.51, 95% CI: 0.37-0.64; SI = 2.21, 95% CI: 1.58-3.07). Higher levels of NL are associated with better HRQOL and lower anxiety among college students. Additionally, anxiety partially mediated the relationship between NL and HRQOL. Furthermore, there is a synergy between NL and anxiety.

Cognitive psychology-based artificial intelligence review.

Most of the current development of artificial intelligence is based on brain cognition, however, this replication of biology cannot simulate the subjective emotional and mental state changes of human beings. Due to the imperfections of existing artificial intelligence, this manuscript summarizes and clarifies that artificial intelligence system combined with cognitive psychology is the research direction of artificial intelligence. It aims to promote the development of artificial intelligence and give computers human advanced cognitive abilities, so that computers can recognize emotions, understand human feelings, and eventually achieve dialog and empathy with humans and other artificial intelligence. This paper emphasizes the development potential and importance of artificial intelligence to understand, possess and discriminate human mental states, and argues its application value with three typical application examples of human-computer interaction: face attraction, affective computing, and music emotion, which is conducive to the further and higher level of artificial intelligence research.

Protective effects of 6-Gingerol on vascular endothelial cell injury induced by high glucose via activation of PI3K-AKT-eNOS pathway in human umbilical vein endothelial cells.

6-Gingerol (6-Gin), an active constituent of Zingiber officinale, has been reported to have anti-inflammatory, anti-oxidative, anti-cancerous etc. bioactivities. However, little is known about its endothelial protective effects and the underlying mechanisms. In this study, our purpose was to investigate the protective effects of 6-Gin and its underlying mechanisms. HUVECs were exposed to high glucose (HG, 33mM glucose) for 48h, followed by 50µM 6-Gin with or without LY294002 (10µM), AKT inhibitor IV (0.5µM) or L-NAME (5mM) for another 24h. Cell viability, levels of NO, LDH and ROS were detected. In addition, the expression levels of IKK, IRS-1, PI3K, AKT, eNOS and their phosphorylated proteins were measured by western blots. Compared with the control, HUVECs were significantly impaired by HG, characterized by decreased levels of the cell viability, NO, pY458-PI3K, pS473-AKT and pS1177-eNOS while increased levels of LDH, pS176-IKK, and p-S312-IRS-1. Conversely, 6-Gin remarkably protected HUVECs against HG-induced injury in a concentration- and time-dependent manner. However, the protective effects of 6-Gin were abolished by co-treatment with LY294002, AKT inhibitor IV or L-NAME at the HG state. Collectively, 6-Gin attenuated the injury of HUVECs induced by HG through the activation of PI3K-AKT-eNOS signal pathway. The findings provide a novel potential for 6-Gin to prevent and treat the angiopathy resulting from diabetes mellitus.

Epigallocatechin-3-gallate inhibits adipogenesis through down-regulation of PPARγ and FAS expression mediated by PI3K-AKT signaling in 3T3-L1 cells.

Epigallocatechin-3-gallate (EGCG), a major component in green tea, functions as extensive bioactivities including anti-inflammation, anti-oxidation, and anti-cancer. However, little is known about its anti-adipogenesis and underlying mechanisms. The purport of this study sought to investigate effects of EGCG on 3T3-L1 preadipocyte differentiation and to explore its possible mechanisms. The 3T3-L1 cells were induced to differentiate under the condition of pro-adipogenic cocktail with or without indicated EGCG concentrations (10, 50, 100, 200µM) for 2, 4, 6 and 8 days, respectively. Also, another batch of 3T3-L1 cells was induced under the optimal EGCG concentration (100µM) with or without SC3036 (PI3K activator, 10µM) or SC79 (AKT activator, 0.5µM) for 8 days. Subsequently, the cell viability was examined by MTT assay and the cell morphology was visualized by Oil red O staining. Finally, the mRNA levels including peroxisome proliferator activated receptor γ (PPARγ) and fatty acid synthase (FAS) were detected by quantitative real time PCR, while the protein levels of PPARγ, FAS, phosphatidylinositol 3 kinase (PI3K), insulin receptor substrate1(IRS1), AKT, and p-AKT were measured by immunoblotting analysis. Our results showed that EGCG inhibited adipogenesis of 3T3-L1 preadipocyte in a concentration-dependent manner. Moreover, the inhibitory effects were reversed by SC3036 or SC79, suggesting that the inhibitory effects of EGCG are mediated by PI3K-AKT signaling to down-regulate PPARγ and FAS expression levels. The findings shed light on EGCG anti-adipogenic effects and its underlying mechanism and provide a novel preventive-therapeutic potential for obesity subjects as a compound from Chinese green tea.

[Osteogenic and adipogenic differentiation of bone marrow multipotent mesenchymal stem cells in the mice with hemorrhagic anemia].

This study was aimed to investigate the effects of osteogenic and adipogenic differentiation of bone marrow multipotent mesenchymal stem cells (MSC) on hematopoiesis. A hemorrhagic anemia mouse model was established by exsanguinating of 0.3 ml blood from angular vein every 1-2 days for 4 weeks. The number of leukocytes, erythrocytes and neutrophils, hemoglobin level, ratio of reticulocyte in peripheral blood and bone marrow cell colony forming unit (CFU) were detected for the identification of the model. The differential potential of MSC in the hemorrhagic anemia mice were identified by CFU-F, histopathologic analysis, and osteogenesis and adipogenesis-related gene expression. The results showed that the erythrocyte numbers of peripheral blood and hemoglobin level decreased in the hemorrhagic anemia mice compared with the control, while the ratio of reticulocyte, the numbers of bone marrow cells and the CFU increased. Furthermore, the numbers of CFU-F, bone marrow hematopoietic cells, and osteogenic cells increased. However, the number of adipocytes decreased. Expressions of osteogenesis-related genes Runx2 and OSX were up-regulated, and adipogenesis-related genes aP2 and PPARγ2 were down-regulated in the hemorrhagic anemia mice compared with the control. It is concluded that the potential of osteogenic differentiation of MSC is enhanced, while the potential of adipogenic differentiation of MSC is weakened in the hemorrhagic anemia mice.

Hematopoietic recovery following chemotherapy is improved by BADGE-induced inhibition of adipogenesis.

This study was designed to investigate the role of increased adipocytes in the bone marrow (BM) niche induced by high-dose chemotherapy in hematopoietic recovery. Arabinosylcytosine (Ara-C) was administered to adult C57BL/6J mice to induce adipogenesis in the BM. We investigated the effects of adipogenesis on hematopoietic recovery following chemotherapy, using the peroxisome proliferator-activated receptor gamma inhibitor, bisphenol A diglycidyl ether (BADGE). Adipocyte hyperplasia could be induced by Ara-C treatment in BM and inhibited by BADGE. The accelerated recovery of leukocyte counts, increased colony forming units, and a higher proportion of Ki67(+)CD45(+) BM cells and Ki67(+)Lin(-)Sca1(+)c-kit(+) hematopoietic stem cells were observed in the long bone marrow of adipocyte-inhibited mice, as well as an increase in the number of CD45(+) BM cells in the tail fatty marrow compared to controls. Adipocytes participated in creating a distinctive niche for hematopoietic cells. In addition, lower expression of stromal cell-derived factor-1α and hypoxia-inducible factor-1 alpha were detected in the BADGE-treated group. These results indicate that hematopoietic recovery is improved following chemotherapy in adipogenesis-inhibited mice. In addition, adipocytes may create an individual niche that affects the proliferation and migration of hematopoietic cells in vitro and in vivo.

[Induction of apoptosis of leukemic tumor cells in mouse model with G-quadruplex ligand Tel03].

This study was aimed to investigate the anti-leukemia activity of Tel03 in vivo. The K562 xenografted leukemia model was established and mice were divided randomly into three groups. Mice of different group were treated with PBS (control), 5 mg/kg Tel03 or 15 mg/kg Tel03 (ip, twice a week) respectively. Tumor volume, body weight and other behavior were observed regularly. Cell apoptosis was detected with TUNEL assay and the expression levels of Bcl-2 and Bax were detected by Western blot. The results indicated that Tel03 exerted anti-leukemia activity in mouse model. Tel03 significantly reduced tumor volume in Tel03-treated group compared with control. In addition, 5 mg/kg Tel03 induced cell apoptosis without exerting apparent toxicity in mice. After Tel03 treatment, the expression of Bcl-2 was inhibited, however, the expression of Bax was up-regulated. It is concluded that G-quadruplex ligand Tel03 can induce cell apoptosis in leukemia mouse model, and this agent may be a potential anticancer drug.