In this study, we investigated the potential effect of onjisaponin B (OB) on aging rats induced by D-gal (D-galactose). Sub-acute aging model was established in rats by the subcutaneous injection of D-gal (120 mg/kg) for 42 days, accompanied with OB (10, 20 mg/kg, p.o.) or normal saline intervention for 28 days since the 14th day after the beginning of D-gal stimulation. Morris water maze test and step-down passive avoidance test were conducted to evaluate the cognitive function of the rats. The superoxidase dismutase (SOD), malondialdehyde (MDA), glutathione (GSH) and glutathione peroxidase (GSH-px) contents in hippocampus were measured by according kits, respectively. And the hippocampus levels of inflammatory mediators including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) were assayed by enzyme-linked immunosorbent assay (ELISA). Furthermore, the expressions of SOD1, MDA5, GSH, GSH-px, NF-кB pathway were present by western blot. It revealed that administration of OB was able to significantly attenuate the D-gal-induced changes in the hippocampus, ranging from cognitive capacity, oxidative stress to inflammation response. In a nutshell, our data provided evidence that OB could contribute to the restoration of cognitive ability by improving the antioxidant and anti-inflammatory capacity in D-gal induced aging rats.
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http://dx.doi.org/10.1016/j.biopha.2018.01.006 | DOI Listing |
PLoS One
January 2025
Department of Nutritional Physiology, National Institute of Medical and Nutritional Sciences "Salvador Zubirán", Mexico City, Mexico.
Childhood obesity increases the risk of developing metabolic diseases in adulthood, since environmental stimuli during critical windows of development can impact on adult metabolic health. Studies demonstrating the effect of prepubertal diet on adult metabolic disease risk are still limited. We hypothesized that a prepubertal control diet (CD) protects the adult metabolic phenotype from diet-induced obesity (DIO), while a high-fat diet (HFD) would predispose to adult metabolic alterations.
View Article and Find Full Text PDFBiogerontology
January 2025
UCIBIO-Applied Molecular Biosciences Unit, Translational Toxicology Research Laboratory, University Institute of Health Sciences (1H-TOXRUN, IUCS-CESPU), 4585-116, Gandra, Portugal.
Sarcopenia and cancer cachexia are two life-threatening conditions often misdiagnosed. The skeletal muscle is one of the organs most adversely affected by these conditions, culminating in poor quality of life and premature mortality. In addition, it has been suggested that chemotherapeutic agents exacerbate cancer cachexia, as is the case of doxorubicin.
View Article and Find Full Text PDFThe dysfunction of mitochondria, the primary source of cellular energy and producer of reactive oxygen species (ROS), is associated with brain aging and neurodegenerative diseases. Scientific evidence indicates that light in the visible and near-infrared spectrum can modulate mitochondrial activity, a phenomenon known in medicine as photobiomodulation therapy (PBM-t). The beneficial effects of PBM-t on dementia and neurodegeneration have been reviewed in the literature.
View Article and Find Full Text PDFDiscov Med
January 2025
Dermatology Department, Beijing Chaoyang Hospital Affiliated to Capital Medical University, 100020 Beijing, China.
Backgrounds: Ultraviolet (UV) radiation-induced photoaging is a multifaceted biological process. Fruit acids have shown promise in combating photoaging. This study aims to investigate the mechanisms underlying the protective effects of fruit acids on UV-induced skin photoaging.
View Article and Find Full Text PDFIran J Basic Med Sci
January 2025
Department of Pharmacology, Faculty of Medicine, Maranatha Christian University, Bandung 40164, West Java, Indonesia.
Objectives: Both intrinsic and extrinsic factors cause skin aging. Intrinsic aging is characterized by decreased collagen density, particularly collagen types I (COL1A1) and III (COL3A1), and an increase in the COL1/COL3 ratio. Extrinsic aging, primarily due to ultraviolet light exposure, leads to photoaging, which causes collagen fragmentation and reduced production, leading to skin sagging.
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