Doxycycline-regulated co-expression of GDNF and TH in PC12 cells.

Current gene therapy models for Parkinson's disease (PD) have adapted two treatment strategies. One is to restore dopamine (DA) production by delivering the genes of DA-synthesizing enzymes such as tyrosine hydroxylase (TH) to the striatum to relieve motor symptoms of PD. Another is to block or slow down progressive degenerative changes by delivering neurotrophic factors such as glial cell line-derived neurotrophic factor (GDNF) to protect the remained neurons.

Up-regulation of the expression of cocaine and amphetamine-regulated transcript peptide by electroacupuncture in the arcuate nucleus of diet-induced obese rats.

It was reported that acupuncture or electro-acupuncture (EA) is effective in reducing the body weight for obese patients, although the mechanisms remain obscure. In a previous study, we have found that rats fed with high-fat (HIF) diet developed diet-induced obesity (DIO) with a concomitant decrease in the hypothalamic content of the cocaine and amphetamine-regulated transcript (CART) peptide, a peptide with anorexiogenic effect. To assess the central effect of EA on DIO rat, we revealed that EA up-regulated the expression of CART peptide in the arcuate nucleus (ARC) of the DIO rats.

A tetracycline-regulatable adeno-associated virus vector for double-gene transfer.

An increasing demand for polycistronic vectors that express multiple genes simultaneously has arisen in recent years to obtain an efficient gene therapy. Armed with the knowledge that the expression of transgene in mammalian cells often requires tight control, we constructed in this study a tetracycline-regulated double-gene adeno-associated virus (AAV) vector carrying green and red fluorescent protein genes and expressed it in PC12 cells. When detected by fluorescence microscope and fluorescence-activated cell sorting, gene expression was induced by 44-66-fold and could be reversibly controlled by doxycycline.

Triptolide protects dopaminergic neurons from inflammation-mediated damage induced by lipopolysaccharide intranigral injection.

Converging lines of evidence suggest that neuroinflammatory processes may account for the progressive death of dopaminergic neurons in Parkinson's disease (PD). Therefore, anti-inflammatory strategies have attracted much interest for their potential to prevent further deterioration of PD. Our previous study showed that triptolide, a traditional Chinese herbal compound with anti-inflammatory and immunosuppressive properties, protected dopaminergic neurons from lipopolysaccharide (LPS)-induced damage in primary embryonic midbrain cell cultures.

[Effect of Chinese herb Tripterygium wilfordii Hook F monomer triptolide on apoptosis of PC12 cells induced by Abeta1-42].

Recent studies indicate that beta-amyloid (Abeta) is the key factor to cause neuronal degeneration in Alzheimer's disease (AD). In the present study, we set up an Abeta induced PC12 cell damage modle and studied the protective effect and related mechanisms of T(10), monomer extracted from Chinese herb Tripterygium wilfordii Hook F. PC12 cells were treated with different concentrations of Abeta (5x10(-4), 5x10(-3), 5x10(-2), 5x10(-1), 5, 50 micromol/L) for 48 h, cell viability was detected by MTT conversion.

Triptolide, a Chinese herbal extract, protects dopaminergic neurons from inflammation-mediated damage through inhibition of microglial activation.

Mounting lines of evidence have suggested that brain inflammation participates in the pathogenesis of Parkinson's disease. Triptolide is one of the major active components of Chinese herb Tripterygium wilfordii Hook F, which possesses potent anti-inflammatory and immunosuppressive properties. We found that triptolide concentration-dependently attenuated the lipopolysaccharide (LPS)-induced decrease in [3H]dopamine uptake and loss of tyrosine hydroxylase-immunoreactive neurons in primary mesencephalic neuron/glia mixed culture.

Triptolide inhibits TNF-alpha, IL-1 beta and NO production in primary microglial cultures.

Microglia are believed to participate in the mediation of neurodegeneration through producing a variety of cytotoxic factors upon activation. Pharmacological intervention in microglial activation may therefore exert a neuroprotective effect. In exploring pharmacological agents that can affect microglial activation, we found in this study that triptolide possesses a powerful inhibitory influence over microglia.