The aim of this study was to investigate the antioxidant and anti-apoptotic activities, as well as the underlying mechanisms of action, of Scrophularia buergeriana ( S. buergeriana ) extract (SBE) in glutamate-induced SH-SY5Y cell death. The roots of S. buergeriana were extracted with 70% ethanol, and standardized SBE was used in this study. To induce cytotoxicity, the SH-SY5Y cells were exposed to glutamate for 3 h, or pre-treated with SBE for 1 h, and subsequently incubated with glutamate for 3 h. The neuro-protective effects were assessed by measuring cell viability and the total glutathione contents using commercial kits. The antioxidant and anti-apoptotic mechanisms of action of SBE were evaluated by western blot analysis. The results confirmed that glutamate-induced toxicity was caused by reactive oxygen species (ROS) production, leading to oxidative stress and DNA damage, thus leading to cell death. However, treatment of the SH-SY5Y cells with SBE significantly increased the viability of the cells exposed to glutamate by upregulating the levels of antioxidant proteins, such as superoxide dismutase (SOD)1, SOD2 and glutathione peroxidase-1 (GPx-1), and directly enhancing the total glutathione contents. Furthermore, SBE attenuated DNA impairment and decreased B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax), cleaved caspase-3 and cleaved poly(adenosine diphosphate (ADP)-ribose) polymerase (PARP) activation. In addition, SBE upregulated Bcl-2 expression via p38 mitogen-activated protein kinases (MAPKs). On the whole, the findings of this study demonstrated that SBE exerts neuroprotective effects against glutamate-induced cell toxicity through its antioxidant and anti-apoptotic activities.
HighlightsCQR-300 inhibited lipid accumulation in 3T3-L1 adipocytes.CQR-300 inhibited the differentiation of adipocytes by regulating adipogenesis.CQR-300 reduced fatty acids and triglyceride accumulation via downregulating lipogenesis.
The aim of the present study was to evaluate the neuroprotective effect of Citrus aurantium extract (cae) and nobiletin against amyloid β 1-42 (aβ 1-42)-induced spatial learning and memory impairment in mice. after injecting aβ 1-42 (5 µl/2.5 min, intracerebroventricular injection), amnesic mice were orally administered cae and nobiletin for 28 days. Memory, spatial and cognitive ability were measured using passive avoidance and a Morris water maze task. acetylcholinesterase (ache) activity was investigated in the hippocampus and cortex using commercial kits and the analysis of Bax, Bcl-2, and cleaved caspase-3 protein expression by western blot assays was used to confirm the anti-apoptotic mechanism of cae and nobiletin. The present study confirmed impairments in learning and memory in the aβ-induced neurodegenerative mice with increased ache activity in the brain. However, the daily administration of CAE and nobiletin reduced the spatial learning deficits and increased the ache activity in the cortex and hippocampus. Furthermore, CAE and nobiletin significantly downregulated the Bax and cleaved caspase-3 protein expression and upregulated the Bcl-2 and Bcl-2/Bax expression in the cortex and hippocampus of aβ-treated mice. These results suggest that cae and nobiletin exert a neuroprotective effect by regulating anti-apoptotic mechanisms, including reduced ache activity in the cortex and hippocampus of the cognitive deficit mouse model.
Over the past decades, periodontitis has become a rising health problem and caused various diseases. In the many studies shows that some extracts and compound to the prevention and treatment of periodontitis. This study focuses on the effects of inhibition of gingival damage and alveolar bone loss. The aim of this study was to evaluate the protective effects of Magnolia biondii extract (MBE) against ligature-induced periodontitis in rats. A ligature was placed around the molar teeth for 8 weeks, and MBE was administered for 8 weeks. Gingival tissue damage and alveolar bone loss were measured by microcomputed tomography (CT) analysis and histopathological examination. Serum Interluekin-1 β (IL-1β), tumor necrosis factor-α (TNF-α), cyclooxygenases-2 (COX-2), and receptor activator of nuclear factor–κB ligand (RANKL) levels were investigated using commercial kits to confirm the antiperiodontitis effects of MBE. We confirmed that ligature-induced periodontitis resulted in gingival tissue damage and alveolar bone loss. However, treatment for 8 weeks with MBE protected from periodontal tissue damage and downregulated serum inflammatory cytokine factors and RANKL levels. These results suggest that MBE exerts antiperiodontitis effects by inhibiting gingival tissue destruction and alveolar bone loss through regulation of anti-inflammatory cytokines in periodontitis-induced rats.
Osteoarthritis (OA) is one of the most well-characterized joint diseases and is associated with chondrocyte inflammation, metalloproteinase upregulation and apoptosis. LI73014F2 is a novel composition prepared from aqueous extract of Terminalia chebula fruit, alcohol extract of Curcuma longa rhizome, and Boswellia serrata extract at 2:1:2 ratio. Earlier studies have shown that LI73014F2 inhibits cyclooxygenase-2 (COX-2), 5-lipoxygenase (5-LOX) activities, and attenuates clinical symptoms in OA subjects. In the present study, we evaluated the protective anti-inflammatory and anti-apoptotic effects, as well as the underlying mechanisms, of LI73014F2 in interleukin (IL)-1β-induced inflammation in human primary chondrocytes. Human chondrocytes were treated with LI73014F2 (0, 12.5, 25 and 50 μg/mL) in IL-1β (10 ng/mL)-containing chondrocyte growth medium for 24 h. Cell viability was assessed using an MTT assay. The pro-inflammatory mediator, inflammatory cytokines, MMPs, apoptosis-related proteins, mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling pathways protein expression levels were detected by western blot analysis. The results demonstrated that LI73014F2 normalized the expressions of COX-2, mPGES-1, PGE2, 5-LOX, LTB4, IL-1β, TNFα, IL-6, MMP-2, MMP-3, MMP-9, MMP-13, Bax/Bcl-2, cleaved caspase-9 and -3, cleaved PARP, phospho-NF-κB p65 and phospho-p38 MAPK proteins in IL-1β-induced primary human chondrocytes. Moreover, the data suggested that LI73014F2 reduced IL-1β-induced inflammation and apoptosis, at least partially via the inhibition of the NF-κB/MAPK signaling pathway. In conclusion, the present findings provide the molecular basis of the anti-OA efficacy of LI73014F2.
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