Effects of Zhichan powder on signal transduction and apoptosis-associated gene expression in the substantia nigra of Parkinson's disease rats

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Abstract

Previous studies have shown that Zhichan powder elevated immunity and suppressed oxidation in mice. Rat models of Parkinson’s disease were induced by stereotaxically injecting 6-hydroxydopamine into the substantia nigra. The rat models were intragastrically treated with Zhichan powder, which is composed of milkvetch root, ginseng, bunge swallowwort root, himalayan teasel root, Magnolia officinalis, Ligustrum lucidum Ait. and szechwan lovage rhizome. Immunohistochemistry and reverse transcription-PCR results demonstrated that mRNA and protein expression of tumor necrosis factor receptor 1, Fas, caspase-8, cytochrome C, Bax, caspase-3, and p53 significantly increased, but Bcl-2 expression significantly decreased in the substantia nigra of rats with Parkinson’s disease. Following Zhichan powder administration, mRNA and protein expression of tumor necrosis factor receptor 1, Fas, caspase-8, cytochrome C, Bax, caspase-3, and p53 diminished, but Bcl-2 expression increased in the rat substantia nigra. These results indicate that Zhichan powder regulates signal transduction protein expression, inhibits apoptosis, and exerts therapeutic effects on Parkinson’s disease.

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Most cited references 29

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TRADD-TRAF2 and TRADD-FADD interactions define two distinct TNF receptor 1 signal transduction pathways.

Hailing Hsu, Hong-Bing Shu, Ming-Gui Pan … (1996)

Tumor necrosis factor (TNF) can induce apoptosis and activate NF-kappa B through signaling cascades emanating from TNF receptor 1 (TNFR1). TRADD is a TNFR1-associated signal transducer that is involved in activating both pathways. Here we show that TRADD directly interacts with TRAF2 and FADD, signal transducers that activate NF-kappa B and induce apoptosis, respectively. A TRAF2 mutant lacking its N-terminal RING finger domain is a dominant-negative inhibitor of TNF-mediated NF-kappa B activation, but does not affect TNF-induced apoptosis. Conversely, a FADD mutant lacking its N-terminal 79 amino acids is a dominant-negative inhibitor of TNF-induced apoptosis, but does not inhibit NF-kappa B activation. Thus, these two TNFR1-TRADD signaling cascades appear to bifurcate at TRADD.

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RNA interference targeting Fas protects mice from fulminant hepatitis.

Erwei Song, Sang-Kyung Lee, Jie Wang … (2003)

RNA interference (RNAi) is a powerful tool to silence gene expression post-transcriptionally. However, its potential to treat or prevent disease remains unproven. Fas-mediated apoptosis is implicated in a broad spectrum of liver diseases, where inhibiting hepatocyte death is life-saving. We investigated the in vivo silencing effect of small interfering RNA (siRNA) duplexes targeting the gene Fas (also known as Tnfrsf6), encoding the Fas receptor, to protect mice from liver failure and fibrosis in two models of autoimmune hepatitis. Intravenous injection of Fas siRNA specifically reduced Fas mRNA levels and expression of Fas protein in mouse hepatocytes, and the effects persisted without diminution for 10 days. Hepatocytes isolated from mice treated with Fas siRNA were resistant to apoptosis when exposed to Fas-specific antibody or co-cultured with concanavalin A (ConA)-stimulated hepatic mononuclear cells. Treatment with Fas siRNA 2 days before ConA challenge abrogated hepatocyte necrosis and inflammatory infiltration and markedly reduced serum concentrations of transaminases. Administering Fas siRNA beginning one week after initiating weekly ConA injections protected mice from liver fibrosis. In a more fulminant hepatitis induced by injecting agonistic Fas-specific antibody, 82% of mice treated with siRNA that effectively silenced Fas survived for 10 days of observation, whereas all control mice died within 3 days. Silencing Fas expression with RNAi holds therapeutic promise to prevent liver injury by protecting hepatocytes from cytotoxicity.

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Caspase 3 activation is essential for efficient influenza virus propagation.

Walter J Wurzer, Oliver Planz, Christina Ehrhardt … (2003)

Apoptosis is a hallmark event observed upon infection with many viral pathogens, including influenza A virus. The apoptotic process is executed by a proteolytic system consisting of a family of cysteinyl proteases, termed caspases. Since the consequences of apoptosis induction and caspase activation for the outcome of an influenza virus infection are not clear, we have addressed this issue by interfering with expression or function of a major virus-induced apoptosis effector, caspase 3. Surprisingly, influenza virus propagation was strongly impaired in the presence of an inhibitor that blocks caspase 3 and in cells where caspase 3 was partially knocked down by small interfering RNAs. Consistent with these findings, poor replication efficiencies of influenza A viruses in cells deficient for caspase 3 could be boosted 30-fold by ectopic expression of the protein. Mechanistically, the block in virus propagation appeared to be due to retention of the viral RNP complexes in the nucleus, preventing formation of progeny virus particles. Our findings indicate that caspase 3 activation during the onset of apoptosis is a crucial event for efficient influenza virus propagation.

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Author and article information

Journal

Journal ID (nlm-ta): Neural Regen Res

Journal ID (iso-abbrev): Neural Regen Res

Journal ID (publisher-id): NRR

Title: Neural Regeneration Research

Publisher: Medknow Publications & Media Pvt Ltd (India )

ISSN (Print): 1673-5374

ISSN (Electronic): 1876-7958

Publication date (Print): 25 September 2012

Volume: 7

Issue: 27

Pages: 2115-2122

Affiliations

[1 ] Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun 130031, Jilin Province, China

[2 ] Department of Immunology, Norman Bethune College of Medicine, Jilin University, Changchun 130021, Jilin Province, China

[3 ] Department of Biochemistry and Molecular Biology, Institute for Regenerative Medicine, Jilin University, Changchun 130021, Jilin Province, China

[4 ] Department of Image, Second Clinical Hospital, Jilin University, Changchun 130021, Jilin Province, China

[5 ] Department of Biotechnology, Life Science College, Jilin University, Changchun 130012, Jilin Province, China

Author notes

Jiajun Chen, Professor, Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun 130031, Jilin Province, China

Corresponding author: Yongmao Liu, Professor, Department of Immunology, Norman Bethune College of Medicine, Jilin University, Changchun 130021, Jilin Province, China; Qingwei Zhou, Associate professor, Department of Biochemistry and Molecular Biology, Institute for Regenerative Medicine, Jilin University, Changchun 130021, Jilin Province, China yongmao@ 123456jlu.edu.cn ; zhouqw@ 123456jlu.edu.cn (N20120319006/YJ)

Author contributions: Yongmao Liu, Jinshu Ma and Yafei Qiu provided the data. Qingwei Zhou integrated the data. Yongmao Liu participated in the study concept and design. Jiajun Chen, Qingwei Zhou and Yongmao Liu analyzed the data. Jiajun Chen, Qingwei Zhou, Yongmao Liu, Ye Kuang, Shihong Yi, Pengguo Zhang and Quan Wan wrote the manuscript. Jiajun Chen and Yongmao Liu were in charge of manuscript authorization. Jinshu Ma and Yafei Qiu participated in the statistical analysis.

Article

Publisher ID: NRR-7-2115

DOI: 10.3969/j.issn.1673-5374.2012.27.005

PMC ID: 4281412

SO-VID: 5e7965a5-752c-4707-88a4-4ae4bcef5a43

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This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Effects of Zhichan powder on signal transduction and apoptosis-associated gene expression in the substantia nigra of Parkinson's disease rats

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Neuronal Signaling

Most cited references 29

TRADD-TRAF2 and TRADD-FADD interactions define two distinct TNF receptor 1 signal transduction pathways.

RNA interference targeting Fas protects mice from fulminant hepatitis.

Caspase 3 activation is essential for efficient influenza virus propagation.

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