ABSTRACT
In this digitalized world, economies have energetically encouraged green transformation. The empirical findings regarding the nexus between human capital and green growth are relatively inconclusive. The study originally explores the effect of human capital on the green growth of a digital economy like China from 1991 to 2019. To investigate the model empirically, we have applied the ARDL technique. Our results indicate that there is a positive impact of different levels of education on the green growth of China in the long run. Regression results also show that renewable energy consumption, internet use, and financial development lead to expansion in green growth in the long run. Our findings can strengthen the belief of the Chinese government on the advancement of green growth.
Subject(s)
Carbon Dioxide , Economic Development , Humans , Carbon Dioxide/analysis , Renewable Energy , ChinaABSTRACT
For Alzheimer's disease (AD), there is still no effective treatment strategy. Pinoresinol diglucoside (PDG) is one of the major lignans isolated from Eucommia ulmoides. It is endowed with multiple pharmacological activities, including anti-inflammatory, antioxidant and anticancer activities. In this study, we investigated the potential neuroprotective functions of PDG in AD. Mice model with AD was established adopting stereotactic hippocampal injection of Aß1-42 (410 pmol/mouse), and 3 days later, mice were administrated with 5 and 10 mg/kg PDG by intragastric administration every day for 3 weeks. Morris water maze and Y-maze tests demonstrated that PDG treatment could markedly reverse Aß1-42-induced memory impairment in mice. It is found that PDG restrained the release of proinflammatory cytokines (tumor necrosis factor α and interleukin 1ß), reactive oxygen species and malondialdehyde, and promoted the activity of the antioxidant enzyme (superoxide dismutase and catalase) by quantitative real-time-PCR, colorimetric method and ELISA assay. Western blot assay results have shown that PDG could also upregulate the ratio of Bcl-2/Bax and downregulate cytochrome c and cleaved caspase-3 expressions, thereby inhibiting neuronal apoptosis. Furthermore, PDG also significantly reduced the expression of Toll-like receptor 4 (TLR4) and the activation of nuclear factor-κB (NF-κB) p65, and promoted nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) expressions. In conclusion, PDG can attenuate neuroinflammation, neuronal apoptosis and oxidative stress through the TLR4/NF-κB and Nrf2/HO-1 pathways, and ameliorate memory dysfunction induced by Aß1-42 in mice.
Subject(s)
Alzheimer Disease/metabolism , Apoptosis/drug effects , Inflammation/metabolism , Lignans/pharmacology , Oxidative Stress/drug effects , Alzheimer Disease/physiopathology , Amyloid beta-Peptides/toxicity , Animals , Catalase/drug effects , Catalase/genetics , Disease Models, Animal , Hippocampus , Injections , Interleukin-1beta/drug effects , Interleukin-1beta/metabolism , Malondialdehyde/metabolism , Mice , Morris Water Maze Test , Peptide Fragments/toxicity , Reactive Oxygen Species/metabolism , Stereotaxic Techniques , Superoxide Dismutase/drug effects , Superoxide Dismutase/genetics , Toll-Like Receptor 4/drug effects , Toll-Like Receptor 4/metabolism , Transcription Factor RelA/drug effects , Transcription Factor RelA/metabolism , Tumor Necrosis Factor-alpha/drug effects , Tumor Necrosis Factor-alpha/metabolismABSTRACT
BACKGROUND The aim of this study was to investigate the protective mechanism of neurovascular unit of Buyang Huanwu decoction (BYHWD) in an Alzheimer's disease (AD) cell model via RAGE/LRP1 pathway and find a reliable target for Alzheimer's disease treatment. MATERIAL AND METHODS Rat brain microvessel endothelial cells (BMECs) were cultured in 10% FBS and 1% penicillin/streptomycin. The AD model was established by administration of 24 µmol/L amyloid-ß peptides 25~35. Different concentrations of BYHWD (0.1 mg/mL, 1 mg/mL, and 10 mg/mL) were added as the drug intervention. The morphology of the cells was observed by light microscopy and the ultrastructure of the cells was observed by microscopy. The inflammatory factors IL-1ß, IL-6, TNF-alpha, and Aß25-35 were detected by ELISA. Flow cytometry was used to assess the apoptosis rate. The expressions of RAGE, LRP1, ICAM-1, VCAM-1, Apo J, Apo E, and NF-kappaBp65 were detected by Western blotting. RESULTS The structure of cells in BYHWDM and BYHWDH gradually recovered with increasing dose. BYHWD decreased the apoptotic rate of BMECs induced by Aß25-35. The cells treated with different concentrations of BYHWD had significant difference in terms of anti-apoptotic effect. The therapeutic effect of BYHWD on AD was via the RAGE/LRP1 and NF-kappaBp65 pathways. CONCLUSIONS BYHWD regulates Aß metabolism via the RAGE/LRP1 pathway, inhibits vascular endothelial inflammation induced by ICAM-1 and VCAM-1 via the NF-kappaBP65 pathway, and promotes morphological changes induced by Aß-induced brain microvascular endothelial cell damage.