Isorhapontigenin prevents β‑amyloid‑associated cognitive impairments through activation of the PI3K/AKT/GSK‑3β pathway.

Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disease that is the most common cause of dementia in the elderly. Aβ1‑42 is significantly associated with memory deficits and it can increase the level of acetylcholine, promote the activity of acetylcholinesterase (AChE), and cause cognitive dysfunction. Isorhapontigenin (ISO) is a stilbene derivative that has antioxidant, anti‑tumor, and anti‑inflammatory effects.

PIAS3 suppresses damage in an Alzheimer's disease cell model by inducing the STAT3-associated STAT3/Nestin/Nrf2/HO-1 pathway.

Background: Alzheimer's disease (AD), the most common form of dementia, is caused by the degeneration of the central nervous system (CNS). A previous study reported that signal transducer and activator of transcription 3 (STAT3) is activated during AD development; nonetheless, the related mechanism remains unknown. Thus, this study used a cell model to explore whether and how the protein inhibitor of activated STAT3 (PIAS3) is involved in AD development.

Inhibition of Long Noncoding RNA SNHG15 Ameliorates Hypoxia/Ischemia-Induced Neuronal Damage by Regulating miR-302a-3p/STAT1/NF-κB Axis.

Purpose: Ischemic brain injury results in high mortality and serious neurologic morbidity. Here, we explored the role of SNHG15 in modulating neuronal damage and microglial inflammation after ischemia stroke.

Materials And Methods: The hypoxia/ischemia models were induced by middle cerebral artery occlusion in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro.

miR-29c-3p inhibits microglial NLRP3 inflammasome activation by targeting NFAT5 in Parkinson's disease.

Microglial inflammation is identified as a key process associated with Parkinson's disease (PD) pathogenesis. Our previous study showed that miR-29c-3p (miR-29c) exhibited anti-inflammatory properties in PD animal and neuronal models. However, the specific role and regulatory mechanism of miR-29c played in microglia are still unclear.

Protective effect of sakuranetin in brain cells of dementia model rats.

Alzheimer's disease (AD) is a high-incidence neurodegenerative disease with complex and diverse pathogenesis. With aging of the population and continuous improvement of living standards, the incidence of AD is on the increase. Therefore, there is need to develop more effective AD drugs in order to improve the quality of life of the elderly.

Roles of Sema3A and VEGF165 in cortical neurons and vascular endothelial cells during oxygen glucose deprivation stimulation.

To investigate the expressions and roles of semaphorin3A (Sema3A) and vascular endothelial growth factor 165 (VEGF165) in cultured rat cortical neurons and vascular endothelial cells after oxygen glucose deprivation (OGD) stimulation. Cultured cortical neurons (NC) and vascular endothelial cells (VEC) of Sprague Dawley (SD) rats (SPF grade) were randomly divided into control group and OGD treatment group. Western blot assay, immunofluorescent staining and immunohistochemical methods were used to determine the expressions of VEGF165, Sema3A and neuropilin-1 (Nrp-1) protein.

Pyridoxine exerts antioxidant effects in cell model of Alzheimer's disease via the Nrf-2/HO-1 pathway.

Pyridoxine is a water- soluble pyridine derivative. The effect of pyridoxine in cell models of Alzheimer's disease (AD), and the potential mechanisms involved, are not fully understood. In this study, the anti-AD effects of pyridoxine were studied in an AD cell model using a combination of techniques viz MTT assay, western blotting and assays for reactive oxygen species (ROS).

Expression changes and roles of Sema3A and Nrp1 in cultured rat cortical neurons after oxygen glucose deprivation.

To investigate the expression changes and roles of Semaphorin3A (Sema3A) and Neuropilin-1 (Nrp1) in cultured rat cortical neurons after oxygen glucose deprivation (OGD). Cultured cortical neurons of newborn SD rats were divided randomly into control group and OGD treatment group. Western blot was performed to detect the expression of Sema3A and Nrp-1 protein and TUNEL was used to detect apoptosis.

Esculetin inhibits oxidative stress and apoptosis in H9c2 cardiomyocytes following hypoxia/reoxygenation injury.

Esculetin (6,7-dihydroxycoumarin), a natural coumarin compound extracted from natural plants, was reported to be involved in ischemia/reperfusion (I/R) injury. However, the role of esculetin in myocardial I/R injury remains unclear. This study was designed to investigate the protective effects of esculetin on cardiomyocytes induced by hypoxia/reoxygenation (H/R), and explore the underlying mechanisms.

IMPA2 polymorphisms and risk of ischemic stroke in a northwest Han Chinese population.

Genetic association analysis has suggested that IMPA2 is a susceptibility gene for ischemic stroke (IS). To explore the association between IMPA2 polymorphisms and the risk of IS in a Han Chinese population, candidate gene association was performed using data from a case-control study of 488 IS patients and 503 control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the association, and associations were evaluated under dominant, recessive, and additive genetic models using PLINK software.

[Effects of Qufengtongluo Recipe on podocin mRNA expression and podocyte morphology in rats with adriamycin-induced nephropathy].

Objective: To observe the effects of Qufengtongluo Recipe (QFTLR) on the expression of podocin mRNA and podocyte morphology in rats with adriamycin-induced nephropathy (AN), and explore the possible mechanism mediating the therapeutic effect of QFTLR on nephropathic proteinuria.

Methods: SD rats were randomized into normal control group, AN model group (established by a single injection of adriamycin via the tail vein), and 3 intervention groups with QFTLR, prednisone, or benazepril treatment. After the corresponding treatments, the expression of podocin mRNA in the renal tissues was detected by RT-PCR methods, and the morphological changes of the podocytes were examined by electron microscope.

[Effects of Qufengtongluo recipe on proteinuria and glomerular filtration membrane in rats with adriamycin-induced nephropathy].

Objective: To assess the therapeutic effect of Qufengtongluo (QFTL) recipe against proteinuria and glomerular filtration membrane damage in rats with adriamycin-induced nephropathy (AN).

Methods: Fifty-six SD rats were randomized into normal control (A) and AN model groups. In the AN model group, the rat AN models established by a single intravenous injection of adriamycin via the tail vein were subdivided into model (B), QFTL recipe (C), prednisone (D), and benazepril (E) groups 3 weeks after adriamycin injection.

[Effects of qufengtongluo recipe on expressions of HSPG mRNA and protein in adriamycin-induced nephropathy rats].

Objective: To investigate the expression of HSPG in glomerular base membrane of adriamycin-induced nephropathy (AN) rats, and the effect of Qufengtongluo recipe on HSPG mRNA expression and proteinuria in AN rats.

Methods: One hundred forty rats were used in this study, including 32 rats in normal control group. AN was induced in the left rats by a single tail intravenous injection of adriamycin.

[Effect of Qufengtongluo recipe on expression of nephrin mRNA in adriamycin-induced nephropathy in rats].

Objective: To investigate the expression of nephrin mRNA in adriamycin-induced nephropathy (AN) in rats, and to explore the effect of Qufengtongluo recipe on proteinuria in AN rats and on the expression of nephrin mRNA.

Methods: Adriamycin nephropathy was induced by a single tail intravenous injection of adriamycin. We randomly divided 140 rats into a normal control group (n=32) and a nephropathy model group (n=108).

[Qufeng Tongluo decoction inhibits lipopolysaccharide-induced rat mesangial cell proliferation in vitro by suppressing NF-kappaB activation and reducing TGF-beta1 and IL-6 mRNA expressions].

Objective: To investigate the effect of Qufeng Tongluo (QFTL) decoction on lipopolysaccharide (LPS)-induced rat mesangial cell proliferation and explore the possible mechanisms underlying the therapeutic effects.

Methods: Thirty-two rats were randomized into normal control, glomerulonephritis model, QFTL treatment and positive control groups, and serum samples were obtained from these groups. Rat mesangial cells with or without LPS exposure were treated with the sera, and the expression of nuclear factor-kappaB (NF-kappaB ) was detected using electrophoretic mobility shift assay (EMSA), and the expressions of transforming growth factor-beta1 (TGF-beta1) and interleukin-6 (IL-6) mRNAs were detected with RT-PCR.

[Effects of Qufeng Tongluo Recipe on proliferation of and TGF-beta1 and IL-6 mRNA expressions in glomerular mesangial cells from rats].

Objective: To investigate the effects of Qufeng Tongluo Recipe (QFTLR), a compound of traditional Chinese herbal medicine for dispelling wind and removing obstruction in the meridians, on cell proliferation and expressions of transforming growth factor-beta1 (TGF-beta1) and interleukin-6 (IL-6) mRNAs induced by lippolysaccharide in glomerular mesangial cells from rats.

Methods: The method of serum pharmacology was used. A total of 32 rats were divided into normal control group, untreated group, QFTLR group and positive control group which also was named Monopril (fosinopril sodium) group.

Study on effect of yishen capsule in preventing recurrence of chronic glomerulonephritis.

Objective: To observe the effect of yishen capsule (YSC) on preventing the recurrence of chronic glomerulonephritis (CGN) and to explore its mechanism preliminarily.

Methods: CGN patients were assigned to the treated group (61 cases) and the control group (48 cases) and all of them were orally administered with 4 mg of Perindopril twice a day, but 3 capsules of YSC, thrice a day, were given additionally to patients in the treated group. The therapeutic course for both groups was 18 months.