Pseudoginsenoside-F11 alleviates oligomeric β-amyloid-induced endosome-lysosome defects in microglia.

Amyloid accumulation in the brain is the major pathological hallmark of Alzheimer disease (AD). Amyloid beta (Aβ) is cleared by the endosomal-autophagy-lysosomal system, which is impaired in AD pathogenesis by an unknown mechanism. Pseudoginsenoside-F11 (PF11), an ocotillol-type ginsenoside, has been demonstrated to decrease the level of Aβ in APP/PS1 mouse brain and to protect neurons by inhibiting the activation of microglia in vitro.

Neurological mechanism of Xiaochaihutang's antidepressant-like effects to socially isolated adult rats.

Objectives: Xiaochaihutang (XCHT) has antidepressant effects in multiple animal models of depression in our previous studies. But the antidepressant effects and exact mechanisms of XCHT in a rat model of chronic social isolation stress (CSIS) have never been studied. We therefore aimed to investigate the effects of XCHT on depressive/anxiety-related behaviours of CSIS-exposed rats and understand the neurological mechanism involving neurogenesis.

SMAD4 suppresses AURKA-induced metastatic phenotypes via degradation of AURKA in a TGFβ-independent manner.

Unlabelled: SMAD4 has been suggested to inhibit the activity of the WNT/β-catenin signaling pathway in cancer. However, the mechanism by which SMAD4 antagonizes WNT/β-catenin signaling in cancer remains largely unknown. Aurora A kinase (AURKA), which is frequently overexpressed in cancer, increases the transcriptional activity of β-catenin/T-cell factor (TCF) complex by stabilizing β-catenin through the inhibition of GSK-3β.

Antidepressant-like effects of Xiaochaihutang in a rat model of chronic unpredictable mild stress.

Ethnopharmacological Relevance: Xiaochaihutang (XCHT) has been used in China for thousands of years to treat "Shaoyang syndrome", which involves depressive-like symptoms. However, few studies have investigated its antidepressant effects and pharmacological mechanism of action. The present study was designed to confirm the antidepressant effect of XCHT using a chronic unpredictable mild stress (CUMS) model and explore its potential mechanism of action by investigating the monoamine neurotransmitters (dopamine and 5-hydroxytryptamine) and neurotrophins (BDNF and NGF).

Neuroprotective effect of pseudoginsenoside-f11 on a rat model of Parkinson's disease induced by 6-hydroxydopamine.

Pseudoginsenoside-F11 (PF11), a component of Panax quinquefolism (American ginseng), plays a lot of beneficial effects on disorders of central nervous system. In this paper, the neuroprotective effect of PF11 on Parkinson's disease (PD) and the possible mechanism were investigated in a rat PD model. PF11 was orally administered at 3, 6, and 12 mg/kg once daily for a period of 2 weeks before and 1 week after the unilateral lesion of left medial forebrain bundle (MFB) induced by 6-hydroxydopamine (6-OHDA).

Xiaochaihutang prevents depressive-like behaviour in rodents by enhancing the serotonergic system.

Objectives: Xiaochaihutang (XCHT) has been used in China for thousands of years to treat 'Shaoyang syndrome', which involves depressive-like symptoms. However, no studies were conducted to demonstrate its antidepressant effect and mechanism. This study was designed to confirm the antidepressant effect of XCHT and explore its mechanism using the pharmacological methods.

Oligomeric Aβ-induced microglial activation is possibly mediated by NADPH oxidase.

Recent studies have shown that oligomeric amyloid-β (oAβ) peptide can potentially activate microglia in addition to inducing more potent neurotoxicity compared with fibrillar Aβ (fAβ); however, its mechanisms of action remain unclear. This study was designed to investigate the possible mechanisms involved in the microglial activation induced by oAβ in BV-2 microglial cells. The results showed that oAβ induced activated properties of microglia, including higher proliferative capacity as well as increased production of reactive oxygen species, nitric oxide (NO), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β).

Effects of cobalt chloride on nitric oxide and cytokines/chemokines production in microglia.

The involvement of microglial activation in metal neurotoxicity is becoming increasingly recognized. Some metal ions, such as zinc (II) and manganese (II), have been recently reported as microglial activators to induce the release of inflammatory mediators including cytokines, chemokines and nitric oxide (NO) which are involved in the pathogenesis of neurological diseases. Cobalt is essential for human life.

Seed Oil of Brucea javanica Induces Apoptotic Death of Acute Myeloid Leukemia Cells via Both the Death Receptors and the Mitochondrial-Related Pathways.

Seed oil of Brucea javanica (BJO) is extracted from the seeds of herb medicine Brucea javanica (L.), and its emulsion formulation (BJOE) has been used clinically to treat carcinomas for many years in China. The antileukemia potential of BJO was investigated in human acute myeloid leukemia cell lines (AML) U937 and HL-60 in vitro and in a mouse U937 xenograft tumor model.

Lesions of nucleus accumbens affect morphine-induced release of ascorbic acid and GABA but not of glutamate in rats.

Our previous studies have shown that local perfusion of morphine causes an increase of extracellular ascorbic acid (AA) levels in nucleus accumbens (NAc) of freely moving rats. Lines of evidence showed that glutamatergic and GABAergic were associated with morphine-induced effects on the neurotransmission of the brain, especially on the release of AA. In the present study, the effects of morphine on the release of extracellular AA, γ-aminobutyric acid (GABA) and glutamate (Glu) in the NAc following bilateral NAc lesions induced by kainic acid (KA) were studied by using the microdialysis technique, coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD) and fluorescent detection (HPLC-FD).

Pituitary adenylate cyclase-activating polypeptide (PACAP) is an upstream regulator of prodynorphin mRNA expression in neurons.

Although dynorphins are widely involved in the control of not only nociceptive neurotransmission but also a variety of brain functions such as memory and emotion, no natural regulator for inducing the mRNA expression of prodynorphin (Pdyn), a precursor protein of dynorphins, is known. Using primary cultures of rat cortical neurons, we found that pituitary adenylate cyclase-activating polypeptide (PACAP), a member of the vasoactive intestinal polypeptide (VIP)/secretin/glucagon neuropeptide family, markedly induces Pdyn mRNA expression. PACAP was much more effective than VIP, indicating a major role for PAC1 in the PACAP-induced Pdyn mRNA expression.

Effect of morphine on brain uracil release in mouse striatum detected by microdialysis.

Effect of acute treatment of morphine is associated with neurotransmitter and neuromodulator changes in the brain. A possible relationship between pyrimidines and morphine has also been discussed. Uracil, a common and naturally occurring pyrimidine derivative which found in RNA, has been suggested to modulate many neurotransmitters or neuromodulators, especially in the mature central nervous system.

Reduction of cyclophosphamide-induced DNA damage and apoptosis effects of ginsenoside Rb(1) on mouse bone marrow cells and peripheral blood leukocytes.

The present study investigated the protective effects of ginsenoside Rb(1) (GRb(1)) against genotoxicity induced by cyclophosphamide (CP). Single cell gel electrophoresis, flow cytometry assay with annexin V-FITC/propidine iodide (PI) and acridine orange (AO)/ethidium bromide (EB) staining assay were employed to measure DNA damage and cell apoptosis, respectively. The activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GPx) and the malondialdehyde (MDA) content were also investigated by a number of colormetric methods.

Synergistic immunostimulatory effect of pidotimod and red ginseng acidic polysaccharide on humoral immunity of immunosuppressed mice.

We investigated the synergistic effect of pidotimod and red ginseng acidic polysaccharide (RGAP) from Panax ginseng C.A. Meyer on humoral immune response challenged by lipopolysaccharide (LPS) and sheep red blood cells (SRBC) in immunosuppressed mice.

Comparison of inhibitory potency of three different curcuminoid pigments on nitric oxide and tumor necrosis factor production of rat primary microglia induced by lipopolysaccharide.

Microglia are the resident innate immune cells in the central nervous system. Evidence supports that the unregulated activation of microglia results in the production of pro-inflammatory cytokines and chemokines that propagate neuronal injury and finally cause neurodegenerative diseases. Curcuminn (Cur), demethoxycurcumin (DMC), and bisdemethoxycurcumin (BDMC) are curcuminoid pigments extracted from turmeric (Curcuma longa L.

Synergistic immunostimulating activity of pidotimod and red ginseng acidic polysaccharide against cyclophosphamide-induced immunosuppression.

We investigated the synergistic effect of combined treatment with red ginseng acidic polysaccharide (RGAP) from Panax ginseng C.A. Meyer and pidotimod in cyclophosphamide-treated mice.

Oxidative DNA damage induced by ethanol in mouse peripheral leucocytes.

It is suggested that reactive oxygen species produced during ethanol intake may induce oxidative DNA damage. The present study, by the use of single cell gel electrophoresis (comet assay), investigated the potential genotoxicity of acute and long-term ethanol administration in mouse peripheral leucocytes. Urinary 8-hydroxy-2'-deoxyguanosine and total antioxidant capacity and reactive oxygen species in whole blood were also detected.

RV09, a novel resveratrol analogue, inhibits NO and TNF-alpha production by LPS-activated microglia.

Excessive activation of microglial cells has been implicated in various neurodegenerative diseases. Resveratrol, a polyphenolic compound found in grapes and wine, has been reported to reduce the activation of microglia. In the present study, 5-[2-(4-bromothiophen-2-yl)vinyl]benzene-1,3-diol (RV09), a novel resveratrol analogue, was found to suppress NO production by LPS-activated N9 microglial cell line and/or cultured rat cortical microglia.

Lesions of the medial prefrontal cortex prevent the acquisition but not reinstatement of morphine-induced conditioned place preference in mice.

In order to further investigate the role of the mPFC in morphine reward and drug priming induced relapse, the present study examined the effects of the mPFC lesions on the acquisition and morphine priming induced reinstatement of conditioned place preference (CPP). In the first experiment, mice received sham or bilateral kainic acid lesions of the mPFC and were subsequently tested for the acquisition of a morphine-induced CPP. In the second experiment, each mouse received lesions of mPFC following the establishment of morphine-induced CPP.

Protective effects of total saponins from stem and leaf of Panax ginseng against cyclophosphamide-induced genotoxicity and apoptosis in mouse bone marrow cells and peripheral lymphocyte cells.

Background: Cyclophosphamide (CP), commonly used anti-cancer, induces oxidative stress and is cytotoxic to normal cells. It is very important to choice the protective agent combined CP to reduce the side effects in cancer treatment. Ginsenosides are biological active constituents of Panax ginseng C.

Protective effects of ginsenoside Rg(3) against cyclophosphamide-induced DNA damage and cell apoptosis in mice.

Despite the significant anti-tumor activities, cyclophosphamide (CP) also shows cytotoxicity to normal cells. In order to explore the protective effects of drugs against CP-induced adverse effects, 20(S)-ginsenoside Rg(3) was tested for its possibly protective activities on CP-induced DNA damage and cell apoptosis in mouse bone marrow cells or peripheral lymphocyte cells. In the current study, the alkaline single cell gel electrophoresis (comet assay), flow cytometry assay with annexin V-FITC/PI and AO/EB staining assay were employed to measure DNA strand breakage and cell apoptosis, respectively.

Direct in vivo evidence of protective effects of grape seed procyanidin fractions and other antioxidants against ethanol-induced oxidative DNA damage in mouse brain cells.

Ethanol is a principle ingredient of alcoholic beverages with potential neurotoxicity and carcinogenicity, and the ethanol-associated oxidative DNA damage in the central nervous system is well documented. The present work studied the possible protective effects of grape seed oligomer and polymer procyanidin fractions against ethanol-induced toxicity and compared these with resveratrol and other well-known antioxidants (ascorbic acid and vitamin E). By using the single cell gel electrophoresis (comet assay), a simple and sensitive technique for genotoxicity studies, the potential genotoxicity of acute and chronic ethanol administration in the different brain regions was investigated.

Anxiolytic-like effects of oleamide in group-housed and socially isolated mice.

Oleamide (cis-9,10-octadecenoamide) is an endogenous sleep-inducing lipid and prototypic member of a new class of biological signaling molecules identified in recent years. In the present study, the anxiolytic-like effect of oleamide was studied in several experimental models of anxiety in group-housed and socially isolated mice. As the results show, socially isolated mice exhibited an anxiogenic-like profile in the elevated plus-maze test, the light/dark test, and the hole-board test, which could be significantly reversed by oleamide (10 or 20 mg/kg, i.

Lesions of the medial prefrontal cortex prevent the induction but not expression of morphine-induced behavioral sensitization in mice.

Repetitive exposure to morphine induces behavioral sensitization, which is supposed to involve in the process of addiction to drugs. As the underlying neuropharmacological mechanisms and anatomical substrates are considerably different between different drugs and different phases of behavioral sensitization, this study was designed to investigate the roles of the medial prefrontal cortex in the induction and expression of morphine-induced behavioral sensitization in mice. In experiments 1 and 2, mice were dosed with morphine (10 mg/kg, i.