Braintone has a therapeutic effect on ischemic brain damage

Main Category: Stroke
Also Included In: Neurology / Neuroscience
Article Date: 19 Aug 2013 - 0:00 PDT Current ratings for:
Braintone has a therapeutic effect on ischemic brain damage

Recently, the importance of the neurovascular unit, which is comprised of neurons, endothelial cells and astrocytes, has received great attention in the field of stroke, because stroke affects not only neurons, but also astrocytes and microvessels.

Within the neurovascular unit, endothelial cells are critical for maintaining normal hemodynamic and metabolic homeostasis. Vascular damage during ischemia often leads to the disruption of the blood-brain barrier and dysregulation of vascular tonus, eventually causing substantial cell death.

The Chinese herbs Rhodiolase, Notoginseng, Folium Ginkgo and Rhizoma Chuanxiong have been used for stroke ancillary treatment in China for years. Braintone contains four major active ingredients: Radix Rhodiolase Essence (a major constituent of Rhodiola rosea L.), Radix Notoginseng Essence, Folium Ginkgo Essence and Rhizoma Chuanxiong.

A recent study published in the Neural Regeneration Research (Vol. 8, No. 19, 2013) combined novel in vivo and in vitro experiments to show that Braintone dose-dependently increased the expression of hypoxia inducible factor 1a, heme oxygenase-1 and vascular endothelial growth factor in the ischemic cortex of rats with middle cerebral artery occlusion. Braintone-containing serum increased levels of hypoxia-inducible factor 1a mRNA and protein, and elevated vascular endothelial growth factor mRNA and heme oxygenase-1 protein expression in a dose-dependent manner in human umbilical vein endothelial cells after glucose-oxygen deprivation.

Collectively, these experimental findings suggest that Braintone has neuroprotective effects on ischemia-induced brain damage via the up-regulation of hypoxia-inducible factor 1a, heme oxygenase-1 and vascular endothelial growth factor expression in vascular endothelial cells.

Article: " Evidence for a therapeutic effect of Braintone on ischemic brain damage " by Yuanyuan Qin1, 2, Yu Luo1, Weiwei Gu1, Lei Yang1, Xikun Shen2, Zhenlun Gu1, Huiling Zhang1, Xiumei Gao3 (1 Department of Pharmacology and Laboratory of Cerebrovascular Pharmacology, College of Pharmaceutical Science, Suzhou Institute of Chinese Meteria Medica, Soochow University, Suzhou 215123, Jiangsu Province, China; 2 Department of Pharmacy, Suzhou Hospital of Traditional Chinese Medicine, Suzhou 215009, Jiangsu Province, China; 3 Department of Anesthesiology, Daxing Hospital, Capital University of Medical Sciences, Beijing 102600, China)

Qin YY, Luo Y, Gu WW, Yang L, Shen XK, Gu ZL, Zhang HL, Gao XM. Evidence for a therapeutic effect of Braintone on ischemic brain damage. Neural Regen Res. 2013;8(19):1743-1755. oi:10.3969/j.issn.1673-5374.2013.19.002

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Mice experience therapeutic changes in glioma after transplantation of neural stem cells

Main Category: Neurology / Neuroscience
Also Included In: Cancer / Oncology;  Stem Cell Research
Article Date: 15 Aug 2013 - 0:00 PDT Current ratings for:
Mice experience therapeutic changes in glioma after transplantation of neural stem cells

Neural stem cells transplanted into tumor-bearing rats can hinder tumor cell growth and proliferation; however, the mechanism remains unclear.

Abnormal activation of the Ras/Raf/Mek/Erk signaling cascade plays an important role in glioma.

Inhibition of this aberrant activity could effectively hinder glioma cell proliferation and promote cell apoptosis.

To investigate the mechanism of glioblastoma treatment by neural stem cell trans-plantation with respect to the Ras/Raf/Mek/Erk pathway, Hua Li and team from the 476 Hospital of Chinese PLA observed Raf-1, Erk and Bcl-2 protein expression as well as Caspase-3 protein expression.

The researchers found that transplantation of neural stem cells could inhibit the abnormal activation of Ras/Raf/Mek/Erk signaling, thus promoting apoptosis and potentially treating glioma.

These findings are published in Neural Regeneration Research (Vol. 8, No. 19, 2013).

Article: " Apoptosis in glioma-bearing rats after neural stem cell transplantation " by Hua Li1, Zhenjun Chen1, Shaopeng Zhou2 (1 Department of Neurology, the 476 Hospital of Chinese PLA, Fuzhou 350002, Fujian Province, China; 2 Department of Anesthesiology, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, Guangdong Province, China)

Li H, Chen ZJ, Zhou SP. Apoptosis in glioma-bearing rats after neural stem cell transplantation. Neural Regen Res. 2013;8(19):1793-1802. doi:10.3969/j.issn.1673-5374.2013.19.007

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Potential cause of Parkinson's disease discovered that points to a new therapeutic strategy

Main Category: Parkinson's Disease
Article Date: 27 Jul 2013 - 0:00 PDT Current ratings for:
Potential cause of Parkinson's disease discovered that points to a new therapeutic strategy

Biologists at The Scripps Research Institute (TSRI) have made a significant discovery that could lead to a new therapeutic strategy for Parkinson's disease.

The findings, recently published online ahead of print in the journal Molecular and Cell Biology, focus on an enzyme known as parkin, whose absence causes an early-onset form of Parkinson's disease. Precisely how the loss of this enzyme leads to the deaths of neurons has been unclear. But the TSRI researchers showed that parkin's loss sharply reduces the level of another protein that normally helps protect neurons from stress.

"We now have a good model for how parkin loss can lead to the deaths of neurons under stress," said TSRI Professor Steven I. Reed, who was senior author of the new study. "This also suggests a therapeutic strategy that might work against Parkinson's and other neurodegenerative diseases."

Genetic Clues

Parkinson's is the world's second-most common neurodegenerative disease, affecting about one million people in the United States alone. The disease is usually diagnosed after the appearance of the characteristic motor symptoms, which include tremor, muscle rigidity and slowness of movements. These symptoms are caused by the loss of neurons in the substantia nigra, a brain region that normally supplies the neurotransmitter dopamine to other regions that regulate muscle movements.

Most cases of Parkinson's are considered "sporadic" and are thought to be caused by a variable mix of factors including advanced age, subtle genetic influences, chronic neuroinflammation and exposure to pesticides and other toxins. But between 5 and 15 percent of cases arise specifically from inherited gene mutations. Among these, mutations to the parkin gene are relatively common. Patients who have no functional parkin gene typically develop Parkinson's-like symptoms before age 40.

Parkin belongs to a family of enzymes called ubiquitin ligases, whose main function is to regulate the levels of other proteins. They do so principally by "tagging" their protein targets with ubiquitin molecules, thus marking them for disposal by roving protein-breakers in cells known as proteasomes. Because parkin is a ubiquitin ligase, researchers have assumed that its absence allows some other protein or proteins to evade proteasomal destruction and thus accumulate abnormally and harm neurons. But since 1998, when parkin mutations were first identified as a cause of early-onset Parkinson's, consensus about the identity of this protein culprit has been elusive.

"There have been a lot of theories, but no one has come up with a truly satisfactory answer," Reed said.

Oxidative Stress

In 2005, Reed and his postdoctoral research associate (and wife) Susanna Ekholm-Reed decided to investigate a report that parkin associates with another ubiquitin ligase known as Fbw7. "We soon discovered that parkin regulates Fbw7 levels by tagging it with ubiquitin and thus targeting it for degradation by the proteasome," said Ekholm-Reed.

Loss of parkin, they found, leads to rises in Fbw7 levels, specifically for a form of the protein known as Fbw7ß. The scientists observed these elevated levels of Fbw7ß in embryonic mouse neurons from which parkin had been deleted, in transgenic mice that were born without the parkin gene, and even in autopsied brain tissue from Parkinson's patients who had parkin mutations.

Subsequent experiments showed that when neurons are exposed to harmful molecules known as reactive oxygen species, parkin appears to work harder at tagging Fbw7ß for destruction, so that Fbw7ß levels fall. Without the parkin-driven decrease in Fbw7ß levels, the neurons become more sensitive to this "oxidative stress" - so that more of them undergo a programmed self-destruction called apoptosis. Oxidative stress, to which dopamine-producing substantia nigra neurons may be particularly vulnerable, has long been considered a likely contributor to Parkinson's.

"We realized that there must be a downstream target of Fbw7ß that's important for neuronal survival during oxidative stress," said Ekholm-Reed.

A New Neuroprotective Strategy

The research slowed for a period due to a lack of funding. But then, in 2011, came a breakthrough. Other researchers who were investigating Fbw7's role in cancer reported that it normally tags a cell-survival protein called Mcl-1 for destruction. The loss of Fbw7 leads to rises in Mcl-1, which in turn makes cells more resistant to apoptosis. "We were very excited about that finding," said Ekholm-Reed. The TSRI lab's experiments quickly confirmed the chain of events in neurons: parkin keeps levels of Fbw7ß under control, and Fbw7ß keeps levels of Mcl-1 under control. Full silencing of Mcl-1 leaves neurons extremely sensitive to oxidative stress.

Members of the team suspect that this is the principal explanation for how parkin mutations lead to Parkinson's disease. But perhaps more importantly, they believe that their discovery points to a broad new "neuroprotective" strategy: reducing the Fbw7ß-mediated destruction of Mcl-1 in neurons, which should make neurons more resistant to oxidative and other stresses.

"If we can find a way to inhibit Fbw7ß in a way that specifically raises Mcl-1 levels, we might be able to prevent the progressive neuronal loss that's seen not only in Parkinson's but also in other major neurological diseases, such as Huntington's disease and ALS [amyotrophic lateral sclerosis]," said Reed.

Finding such an Mcl-1-boosting compound, he added, is now a major focus of his laboratory's work.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our parkinson's disease section for the latest news on this subject.

“Parkin-Dependent Degradation of the F-box protein Fbw7 ß Promotes Neuronal Survival in Response to Oxidative stress by Stabilizing Mcl-1,” Susanna Ekholm-Reed, Matthew S. Goldberg, Michael G. Schlossmacher and Steven I. Reed, Published ahead of print 15 July 2013, doi: 10.1128/MCB.00535-13

Funding for the study was provided in part by the National Institutes of Health (NS059904 and CA078343).

Scripps Research Institute

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