shikonin has been researched along with Cognitive-Dysfunction* in 2 studies
2 other study(ies) available for shikonin and Cognitive-Dysfunction
Article | Year |
---|---|
Systemic administration of Shikonin ameliorates cognitive impairment and neuron damage in NPSLE mice.
Shikonin is an anti-inflammatory natural herbal drug extracted from Lithospermum erythrorhizon and its therapeutic effect on neuropsychiatric systemic lupus erythematosus (NPSLE) is yet unknown. In our study, Shikonin significantly reversed the cognitive impairment and alleviated the brain tissue damage in NPSLE mice. The permeability of blood-brain barrier was also verified to be repaired in Shikonin-treated NPSLE mice. In particular, we found that Shikonin alleviated neuroinflammation through inhibiting β-catenin signaling pathway, thereby depressing the activation of microglia and the loss of neuronal synapses. Overall, Shikonin may be a promising candidate drug for NPSLE through diminishing neuroinflammation and repairing neuron damage. Topics: Animals; Anti-Inflammatory Agents; Cognitive Dysfunction; Lupus Erythematosus, Systemic; Lupus Vasculitis, Central Nervous System; Mice; Neuroinflammatory Diseases; Neurons | 2023 |
Shikonin ameliorates D-galactose-induced oxidative stress and cognitive impairment in mice via the MAPK and nuclear factor-κB signaling pathway.
Oxidative stress acts as the major causative factor for various age-associated neurodegenerative diseases, triggering cognitive and memory impairments. In the present study, the underlying neuroprotective mechanism governing how shikonin acts against D-galactose (D-gal)-induced memory impairment, neuroinflammation and neuron damage was examined. The results revealed that chronic administration of D-gal [150 mg/kg intraperitoneally (i.p.)] in mice caused cognitive and memory impairments, as determined by Morris water-maze test. Shikonin treatment, however, alleviated D-gal-induced memory impairment and reversed the D-gal-induced neural damage and apoptosis. Furthermore, western blotting and the results of morphological analysis revealed that shikonin treatments markedly reduced D-gal induced neuroinflammation through inhibition of astrocytosis as determined by glial fibrillary acidic protein (GFAP) detection, and downregulating other inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Moreover, shikonin treatment led to inhibition of the activation of nuclear factor-κB (NF-κB) and the phosphorylation of mitogen-activated protein kinases (MAPKs), preventing neurodegeneration. Hence, taken together, the results of the present study suggested that shikonin attenuated D-gal-induced memory impairment, neuroinflammation and neurodegeneration, possibly via the NF-κB/mitogen-activated protein kinase (MAPK) pathway. Our data suggest that shikonin could be a promising, endogenous and compatible antioxidant candidate for age-associated neurodegenerative diseases, including Alzheimer's disease. Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Cells, Cultured; Cognitive Dysfunction; Cytokines; Extracellular Signal-Regulated MAP Kinases; Galactose; Humans; Inflammation Mediators; Male; Mice; Mice, Inbred C57BL; Naphthoquinones; Neurodegenerative Diseases; Neurogenic Inflammation; NF-kappa B; Oxidative Stress; Signal Transduction | 2020 |