Background. Tongnao decoction (TND) has been extensively prescribed for the treatment of stroke. However, little is known about the role of TND in the progression of carotid atherosclerosis. Methods. A mouse carotid atherosclerosis model was established with a silastic collar placed around the right common carotid artery and fed on Western diet for 12 weeks. The treatment group was given a gavage of TND at a dose of 1 mg/kg/d. The atherosclerotic lesion size and the compositions were observed using Oil red O staining and immunofluorescent staining. Enzyme-linked immunosorbent assay (ELISA) was used to evaluate the levels of lipid profiles, oxidative stress, and inflammatory factors. Human aortic endothelial cells (HAoECs) were treated with oxLDL with or without TND for in vitro experiments. Results. TND treatment significantly suppressed the progression of atherosclerosis, as characterized with a smaller lesion size, less percentage of vascular smooth muscle cell proliferation, endothelial cell apoptosis, and macrophage infiltration. In addition, TND decreased the levels of lipid profiles, oxidative stress, and inflammatory factors in atherosclerosis. In vitro results showed that TND inhibited the apoptosis of endothelial cells via activating ERK and AKT pathway. Conclusions. Our study demonstrated that TND significantly protected from atherosclerosis via promoting endothelial cell survival and alleviating oxidative stress and inflammatory response, which may have become a treatment in atherosclerotic diseases.
Alzheimer’s disease (AD) is one of neurodegenerative diseases characterized by cognitive and memory decline, accompanying with neurofibrillary tangles (NFTs) made of hyperphosphorylated tau protein and senile plaques (SP) accumulated by β-amyloid protein (Aβ).
BAY 73-6691, an inhibitor of phosphodiesterase-9 (PDE-9), can improve learning and memory of elderly rats. However, the effects of BAY 73-6691 on neuroapoptotic and neuroinflammatory events, as well as synaptic plasticity of differentiated PC12 cells are remain unclear. In this work, we screened
apoptotic cells induced by Aβ25-35 via flow cytometry. TNF-α, IL-1β, IL-6 secreted by PC12 cells were estimated by ELISA kits. The levels of cGMP, PKG and CREB mediated by BAY 73-6691 were assessed. Moreover, we conducted western blots analysis
to evaluate the phosphorylation of tau and synaptic related proteins. Results showed that BAY 73-6691 could reduce Aβ25-35-triggered neuroapoptosis and neuroinflammation. Phosphorylation of tau was inhibited by BAY 73-6691, whereas sildenafil citrate (SC, an inhibitor
of cGMP) partially weakened the effect of BAY 73-6691. Additionally, synaptic plasticity restored by BAY 73-6691 was also suppressed via SC. Taken together, BAY 73-6691 exhibited neuro protective effects, and altered tau phosphorylation as well as synaptic related proteins through cGMP/PKG/CREB
pathway.
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