Ethnopharmacological Relevance: Dangguisusan (DGSS) is a widely used prescription for the treatment of traumatic injury in Korean medicine.
Aim Of The Study: To demonstrate the effects of DGSS on a mouse model of traumatic brain injury (TBI) for providing scientific evidence in clinical use.
Materials And Methods: TBI was induced in a mouse model using the controlled cortical impact method. Water extract of DGSS (50, 150, and 450 mg/kg) was administered twice a day for 8 d. Histological analyses were performed 8 d after TBI. Moreover, beam-walking, grip-strength, and novel object recognition (NOR) tests were conducted to evaluate the effects on motor function, muscle strength, and cognitive memory function, respectively.
Result: DGSS inhibited body weight loss, hippocampal damage, and neuronal loss in the thalamic region. Furthermore, it reduced transverse time and foot faults in the beam-walking test at 3 d and increased the muscle strength in the grip-strength test at 3 and 8 d. It also improved the recognition index (%) in the NOR test. However, DGSS did not show protective effects against total damage.
Conclusions: DGSS might improve sensory-motor and cognitive functions after TBI with partial protective effects against brain damage. The present findings provide a scientific basis for the clinical use of DGSS in TBI.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.jep.2018.07.015 | DOI Listing |
Blood
January 2025
State Key Laboratory of Experimental Hematology, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College; Center for Stem Cell Medicine,, Tianjin, China.
Adenosine-to-inosine (A-to-I) RNA editing is a prevalent RNA modification essential for cell survival. The process is catalyzed by the Adenosine Deaminase Acting on RNA (ADAR) enzyme family that converts adenosines in double-stranded RNAs (dsRNAs) into inosines, which are read as guanosines during translation. Deep sequencing has helped to reveal that A-to-I editing occurs across various types of RNAs to affect their functions.
View Article and Find Full Text PDFBlood
January 2025
Cleveland Clinic, Cleveland, Ohio, United States.
Antibodies to β2-glycoprotein I (β2GPI) cause thrombosis in antiphospholipid syndrome, however the role of β2GPI in coagulation in vivo is not understood. To address this issue, we developed β2GPI-deficient mice (Apoh-/-) by deleting exon 2 and 3 of Apoh using CRISPR/Cas9 and compared the development of thrombosis in wild-type (WT) and Apoh-/- mice using rose bengal and FeCl3-induced carotid thrombosis, laser-induced cremaster arteriolar injury, and inferior vena cava (IVC) stasis models. We also compared tail bleeding times and activation of platelets from WT and Apoh-/- mice in the absence and presence of β2GPI.
View Article and Find Full Text PDFStroke
February 2025
Neurovascular Research Unit, Pharmacology Department, Complutense Medical School, Instituto Investigación Hospital 12 Octubre, Madrid, Spain (G.D., B.D., A.M., J.M.P., I.L.).
Background: Acute ischemic stroke treatment typically involves tissue-type plasminogen activator (tPA) or tenecteplase, but about 50% of patients do not achieve successful reperfusion. The causes of tPA resistance, influenced by thrombus composition and timing, are not fully clear. Neutrophil extracellular traps (NETs), associated with poor outcomes and reperfusion resistance, contribute to thrombosis.
View Article and Find Full Text PDFBiosci Rep
January 2025
Scotland's Rural College Animal and Veterinary Sciences Research Group, Edinburgh, United Kingdom.
Approximately one in every 800 children is born with the severe aneuploid condition of Down Syndrome, a trisomy of chromosome 21. Low blood pressure (hypotension) is a common condition associated with DS and can have a significant impact on exercise tolerance and quality of life. Little is known about the factors driving this hypotensive phenotype and therefore therapeutic interventions are limited.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Kidney Disease Center, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
METTL3, a key enzyme in N6-methyladenosine (m6A) modification, plays a crucial role in the progression of renal fibrosis, particularly in chronic active renal allograft rejection (CAR). This study explored the mechanisms by which METTL3 promotes renal allograft fibrosis, focusing on its role in the macrophage-to-myofibroblast transition (MMT). Using a comprehensive experimental approach, including TGF-β1-induced MMT cell models, METTL3 conditional knockout (METTL3 KO) mice, and renal biopsy samples from patients with CAR, the study investigates the involvement of METTL3/Smad3 axis in driving MMT and renal fibrosis during the episodes of CAR.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!