New Tiaoxin Recipe Alleviates Energy Metabolism Disorders in an APPswe/PS1DE9 Mouse Model of Alzheimer's Disease.

Background: Alzheimer's disease (AD) is a typical neurodegenerative disease with a complex etiology. Until now, there has been no effective treatment available for AD; however, improving energy dysmetabolism, the key pathological event in the early stage of AD, can effectively delay the progression of AD.

Objective: This paper aims to investigate the therapeutic effect and potential mechanism of the new Tiaoxin recipe on early AD.

Aβ promotes CD38 expression in senescent microglia in Alzheimer's disease.

Background: In Alzheimer's disease (AD), the neuroinflammatory response mediated by the activation of senescent microglia is closely related to energy dysmetabolism. However, the mechanism underlying the interaction between the energy metabolism of aging microglia and neuroinflammation remains unclear.

Methods: We used biochemical methods, enzyme-linked immunosorbent assay (ELISA), immunofluorescence, and western blot to determine the effects and mechanism of CD38 knockdown on energy metabolism and neuroinflammation in Aβ1-40 injured BV2 cells.

Effect of BuShen JiangZhi Recipe on Atherosclerosis in ApoE Mice by Regulating the Expression of Anpep via mmu_circRNA_22187.

The BuShen JiangZhi (BSJZ) recipe is a Chinese medicine compound with the effect of tonifying the kidney, replenishing essence, and lowering blood fat to unblock vessels. The purpose of this study is to explore whether the mechanism of BSJZ for effective intervention in the treatment of AS is related to mmu_circRNA_22187 and aminopeptidase N (Anpep). ApoE mice were induced by a high-fat diet to replicate the AS model.

Fisetin ameliorates atherosclerosis by regulating PCSK9 and LOX-1 in apoE mice.

The purpose of the current study was to investigate the mechanism by which fisetin improves atherosclerosis (AS) by regulating lipid metabolism and senescence in apolipoprotein E-deficient (apoE) mice. An AS model was established by feeding apoE mice a high-fat diet. Mice were randomly divided into the model group (n=18), the fisetin group (n=18) and the atorvastatin group (n=18).

Bushen Jiangzhi formula reduces atherosclerosis in apoE-/- mice through autophagy.

Objective: To study the effect of Bushen Jiangzhi formula (BSJZF) on atherosclerosis (AS) in apolipoprotein E knockout (apoE-/-) mice and the underlying mechanism.

Methods: We used a high fat diet to induce AS in apoE-/- mice. The mice were randomly divided into four groups: model, BSJZF, atorvastatin, and 3-methyladenine groups.

Efficacy of Shoushen granule on adenosine triphosphate binding cassette transporter A1, proprotein convertase subtilisin/kexin type 9 and toll-like receptor 4/nuclear factor kappa-B signaling pathway in ApoE-knockout mice.

Objective: To evaluate the efficacy of Shoushen granule, prepared with four Chinese medicinals, on the targeted regulation of adenosine triphosphate binding cassette transporter A1 (ABCA1) through proprotein convertase subtilisin/kexin type 9 (PCSK9) and toll-like receptor 4 (TLR4) / nuclear factor kappa-B (NF-κB) signaling pathway to affect atherosclerosis (AS) in ApoE-knockout (ApoE-/-) mice.

Methods: ApoE-/- mice fed with a high-fat diet were used for AS modeling and divided into Model, Shoushen, and Atorvastatin groups. C57BL/6J mice at the same age and background strain were included in the Control group.

Quercetin Suppresses the Progression of Atherosclerosis by Regulating MST1-Mediated Autophagy in ox-LDL-Induced RAW264.7 Macrophage Foam Cells.

Objective: To investigate the process by which quercetin suppresses atherosclerosis by upregulating MST1-mediated autophagy in RAW264.7 macrophages.

Methods: An in vitro foam cell model was established by culturing RAW264.

Nicotinamide phosphoribosyltransferase‑related signaling pathway in early Alzheimer's disease mouse models.

Alzheimer's disease (AD) is a neurodegenerative disease of the central nervous system that is characterized by progressive cognitive dysfunction and which ultimately leads to dementia. Studies have shown that energy dysmetabolism contributes significantly to the pathogenesis of a variety of aging‑associated diseases and degenerative diseases of the nervous system, including AD. One focus of research thus has been how to regulate the expression of nicotinamide phosphoribosyltransferase (NAMPT) to prevent against neurodegenerative diseases.

Fisetin, via CKIP-1/REGγ, limits oxidized LDL-induced lipid accumulation and senescence in RAW264.7 macrophage-derived foam cells.

To test the hypothesis that the flavonoid compound, fisetin, protects macrophages from lipid accumulation and senescence through regulation of casein kinase 2-interacting protein-1 (CKIP-1)/REGγ (11S regulatory particles, 28 kDa proteasome activator, proteasome activator subunit 3) signaling. RAW264.7 macrophage cells were exposed to 100 μg/ml oxidized low-density lipoprotein (ox-LDL) with or without 20 μg/ml fisetin for 24 h.

Quercetin has a protective effect on atherosclerosis via enhancement of autophagy in ApoE mice.

The present study examined the involvement of autophagy as a mechanism in the protective effect of quercetin (QUE) on atherosclerosis (AS) in ApoE mice. An AS model was established by feeding ApoE mice a high-fat diet (HFD). Mice were divided into four experimental groups: The model, QUE, 3-methyladenine (3-MA) and QUE + 3-MA groups.

Tiaoxin Recipe, a Chinese herbal formula, inhibits microRNA-34a expression in the APPswe/PS1ΔE9 mouse model of Alzheimer's disease.

Objective: To investigate the effect and underlying mechanisms of Tiaoxin Recipe (a Chinese herbal formula) treatment on Alzheimer's disease (AD).

Methods: Twelve-week-old APPswe/PS1ΔE9 (APP/PS1) double transgenic mice were used as a model of AD-afflicted mice. One group of mice was treated with Tiaoxin Recipe by gastrogavage for 12 weeks, while two other groups were given intraperitoneal injections of nicotinamide adenine dinucleotide or FK866 for 4 weeks.

Quercetin protects against atherosclerosis by regulating the expression of PCSK9, CD36, PPARγ, LXRα and ABCA1.

The aim of this study was to investigate the mechanisms through which quercetin protects against atherosclerosis (AS) in apoE‑/‑ mice by regulating the expression of proprotein convertase subtilisin/kexin type 9 (PCSK9), cluster of differentiation 36 (CD36), peroxisome proliferator‑activated receptor γ (PPARγ), liver X receptor α (LXRα) and ATP binding cassette transporter A1 (ABCA1). We established an animal model of high‑fat diet induced AS using apoE‑/‑ mice. H&E, Oil Red O and Masson's trichrome staining were performed on aortic sinus and liver tissue sections to evaluate the histopathology, lipid accumulation and collagen deposition, respectively.

Effect of Quercetin on Atherosclerosis Based on Expressions of ABCA1, LXR-α and PCSK9 in ApoE Mice.

Objective: To investigate the effect of quercetin on ATP binding cassette transporter A1 (ABCA1), liver X receptor (LXR), and proprotein convertase subtilisin/kexin type 9 (PCSK9) expressions in apoE-knockout (ApoE) mice.

Methods: The high-fat diet-induced atherosclerosis (AS) in ApoE mice was established. Thirty-six mice were divided into 3 groups using random number table method: model group (n=12), quercetin group (n=12), and atorvastatin group (n=12), with C57BL/6J mice of the same strain and age as the control group (n=12).

Salidroside slows the progression of EA.hy926 cell senescence by regulating the cell cycle in an atherosclerosis model.

Aging is the major risk factor for diseases of the cardiovascular system, such as coronary atherosclerotic heart disease, but little is known about the relationship between atherosclerosis (AS) and age‑related declines in vascular structure and function. Here, we used histological analyses in combination with molecular biology techniques to show that lipid deposition in endothelial cell was accompanied by aging and growth arrest. Endothelial cell senescence is sufficient to cause AS; however, we found that salidroside reduced intracellular lipid deposition, slowed the progression of endothelial cell senescence and inhibited the expression of the senescence‑related molecules and phosphorylated the retinoblastoma (Rb) protein.

Effect of the herbal formulation Shen-Zhi-Ling on an APP/PS1 mouse model of Alzheimer's disease by modulating the biliverdin reductase/heme oxygenase 1 system.

Shen-Zhi-Ling (SZL) oral liquid is a traditional Chinese medicine formula that is mainly used for the clinical treatment of mild to moderate Alzheimer's disease (AD). The aim of the present study was to investigate the effects and underlying mechanisms of SZL treatment on AD. APP/PS1 transgenic mice were utilized to evaluate the effect of SZL treatment (0.

Salidroside protects PC12 cells from Aβ1‑40‑induced cytotoxicity by regulating the nicotinamide phosphoribosyltransferase signaling pathway.

Alzheimer's disease (AD) is the most common type of senile dementia, which often develops in elderly or presenile individuals. As one of the pathological features of AD, amyloid β‑protein (Aβ) causes energy dysmetabolism, thereby inducing cellular damage and apoptosis. Salidroside is the main active component of the traditional Chinese medicine Rhodiola.

Effect of Shoushen granule on arterial elasticity in patients with carotid atherosclerosis: a clinical randomized controlled trial.

Objective: To investigate the effectiveness of Shoushen granule, Chinese herbal preparation, on carotid artery elasticity in patients with carotid atherosclerosis.

Methods: The total of 156 carotid atherosclerosis patients were randomly divided into the intervention group (83 cases, treated with Shoushen granule) and the control group (73 cases, treated with pravastatin). Brachial-ankle pulse wave velocity baPWV) and Ankle-Brachial Pressure Index (ABI) were measured by automated arteriosclerosis detector.

Adiponectin gene polymorphisms contributes to ischemic stroke risk: A meta-analysis.

Background: Previous studies have reported the relation between the adiponectin polymorphisms and the risk of ischemic stroke. However, the findings is inclusive. In the present study, we performed a meta-analysis to clarify the relation between the adiponectin polymorphisms and the stroke.

Early induction of oxidative stress in a mouse model of Alzheimer's disease with heme oxygenase activity.

Evidence suggests that brain tissues of patients with Alzheimer's disease (AD) are easily attacked by oxidative stress, and numerous studies indicate that heme oxygenase (HO) is a major cell adaptive responder to stress. However, whether HO‑1 and HO‑2 play different roles in this process has not yet been studied. In the present study, it was shown in an AD model that HO‑1 and HO‑2 have different roles in the early stages of AD.

Regulation of neuronal toxicity of β-amyloid oligomers by surface ATP synthase.

Alzheimer disease (AD) is characterized by the accumulation of amyloid-β (Aβ) protein and intracellular neurofibrillary tangles. Previous studies have shown that Aβ aggregation is one of the most important initiating factors in the pathogenesis of AD. Oligomers of Aβ cause neurotoxicity, synaptic dysfunction and memory impairments that underlie AD.

Attenuation of exogenous angiotensin II stress-induced damage and apoptosis in human vascular endothelial cells via microRNA-155 expression.

Numerous studies have indicated that cells and tissues have means of blocking their response to continuous stress signals to protect themselves from damage. Overexpression of angiotensin II (Ang II) in the renin-angiotensin system can cause vascular endothelial damage, but the mechanism of adjustment of the dynamic equilibrium remains unclear. In this study, we investigated whether microRNA-155 (miR-155) can suppress continuous Ang II stress signals that would otherwise cause vascular endothelial damage.

[Chinese herbal medicine for patients with mild to moderate Alzheimer disease based on syndrome differentiation: a randomized controlled trial].

Background: Alzheimer disease (AD) is a chronic neurodegenerative disease that is characterized by its gradual progression. At present, the cause and mechanism of AD are yet unclear, and there is no effective therapy for treating it. With development of global aging, the prevalence rate of AD is increasing.

β-amyloid peptide binds and regulates ectopic ATP synthase α-chain on neural surface.

Accumulation of the amyloid β protein (Aβ) in the brain is an important step in the pathogenesis of Alzheimer's disease. Many molecules could bind with Aβ, among which some molecules mediate Aβ neuronal toxicity. Thus, it is of interest to study the binding proteins of Aβ, and the functions that might be affected by Aβ.

Neuroprotective effects of Buyang Huanwu decoction against hydrogen peroxide induced oxidative injury in Schwann cells.

Ethnopharmacological Relevance: Buyang Huanwu decoction (BYHWD) is a traditional Chinese medicine and can be used to promote peripheral nerve regeneration. However the regenerative mechanism of BYHWD remains unclear. The objective of this study was to investigate the protective mechanisms of BYHWD in Schwann cells damaged by hydrogen peroxide (H(2)O(2)).

Neuronal cell surface ATP synthase mediates synthesis of extracellular ATP and regulation of intracellular pH.

The ATP synthase is known to play important roles in ATP generation and proton translocation within mitochondria. Here, we now provide evidence showing the presence of functional ecto-ATP synthase on the neuronal surface. Immunoblotting revealed that the α, β subunits of ATP synthase F1 portion are present in isolated fractions of plasma membrane and biotin-labelled surface protein from primary cultured neurons; the surface distribution of α, β subunits was also confirmed by immunofluorescence staining.