Objective: To explore the effect of extract of Ginkgo biloba (EGb) on vascular endothelial dysfunction induced by AGEs and to investigate the potential mechanisms.
Methods: Exogenous glycosylated bovine serum Albumin (AGEs-BSA) was prepared according to the methods of article. Vascular endothelial dysfunction was induced by tail vein injection of AGEs-BSA. The treatment group rats were given tail vein injections with AGEs-BSA followed by immediate intragastric of EGb (15,30 mg/kg/day, respectively) for 30 days. At the end of 30 days period, rats were anaesthetized with an intraperitoneal injection of sodium pentobarbital. Blood samples were collected from the carotid artery for biochemical assay of NO, MDA, SOD, DDAH, ADMA. The thoracic aorta was immediately isolated and cut into rings of 3 - 4 mm. Then ACh-induced EDR response and sodium SNP-induced endothelium-independent relaxation of aortic rings were examined.
Results: Results from in vivo experiments showed that the injection of AGEs-BSA significantly inhibited ACh-induced EDR response, but had no effect on SNP-induced endothelial-independent relaxation. The injection of AGEs-BSA decreased concentration of serum NO, activity of serum SOD and elevated serum MDA and ADMA level. Egb markedly attenuated AGEs-BSA induced inhibition of EDR response, increase of serum MDA and ADMA level, reduction of both NO level and activity of serum SOD.
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Cell Commun Signal
January 2025
School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
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BMC Genomics
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State Key Laboratory of Biocontrol, Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), China-ASEAN Belt and Road Joint Laboratory on Mariculture Technology, Guangdong Provincial Key Laboratory of Aquatic Economic Animals, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Infectious spleen and kidney necrosis virus (ISKNV) is a highly virulent and rapidly transmissible fish virus that poses threats to the aquaculture of a wide variety of freshwater and marine fish. N6-methyladenosine (mA), recognized as a common epigenetic modification of RNA, plays an important regulatory role during viral infection. However, the impact of mA RNA methylation on the pathogenicity of ISKNV remains unexplored.
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Zhengzhou Key Laboratory of Cardiovascular Aging, Henan Province Key Laboratory for Prevention and Treatment of Coronary Heart Disease, National Health Commission key Laboratory of Cardiovascular Regenerative Medicine, Central China Fuwai Hospital of Zhengzhou University, Fuwai Central China Cardiovascular Hospital & Central China Branch of National Center for Cardiovascular Diseases, Zhengzhou, Henan, China.
N6-adenosine methylation (m6A) of RNA is involved in the regulation of various diseases. However, its role in chemotherapy-related vascular endothelial injury has not yet been elucidated. We found that methyltransferase-like 3 (METTL3) expression was significantly reduced during doxorubicin (DOX)-induced apoptosis of vascular endothelial cells both in vivo and in vitro, and that silencing of METTL3 further intensified this process.
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January 2025
Department of Ophthalmology, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, 02111, USA.
Activation of anaplerosis takes away glutamine from the biosynthetic pathways to the energy-producing TCA cycle. Especially, induction of hyperoxia driven anaplerosis in neurovascular tissues such as the retina during early stages of development could deplete biosynthetic precursors from newly proliferating endothelial cells impeding physiological angiogenesis and leading to vasoobliteration. Using an oxygen-induced retinopathy (OIR) mouse model, we investigated the metabolic differences between OIR-resistant BALB/cByJ and OIR susceptible C57BL/6J strains at system levels to understand the molecular underpinnings that potentially contribute to hyperoxia-induced vascular abnormalities in the neural retina.
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