06.12.13
GMP-certified tocotrienol producer Carotech Inc. announced an NIH-funded study published recently in the Journal of Cerebral Blood Flow and Metabolism, that sheds light on how tocotrienol, a 12-Lox inhibitor, acts to confer neuroprotection post-stroke.
In the study, Professor Chandan K. Sen and his team of researchers at The Ohio State University Wexner Medical Center, Columbus, USA, elucidated the mechanisms of microRNA precursor (miR29) in stroke-induced neuronal injuries. They showed that alpha-tocotrienol (Tocomin, Carotech Inc.) prevented miR29 loss at the infarct site during stroke and therefore protected the neurons from cell death (apoptosis).
“Micro RNAs (miR) are small non-coding RNA molecules that play important role in regulating gene expression at the translation level, and miR29 is the micro RNA in the study of stroke etiology and in many other neurodegenerative disorders including Alzheimer’s Disease,” said Dr. Savita Khanna, co-researcher of the study, at the recently concluded Palm International Nutraceutical Conference at Kuala Lumpur.
The miR29 family of genes - miR29a, miR29b1, miR29b2 (collectively miR29b) and miR29c in the human genome plays an important role in regulating gene expression. MiR29b isrecognized as a neuronal survival factor. Specific loss of miR-29b at the infarct site after stroke leads to neuronal cell death. As such, prevention of such stroke-induced loss of miR-29b significantly improves stroke outcomes.
The researchers used the mouse stroke model, where mice were subjected to temporary middle-cerebral artery occlusion (MCAO) to induce stroke. At 48 hours after MCAO, there was a significant loss of miR29b at the infarct site.
By re-introducing miR29b at the infarct site, it decreased stroke-induced brain lesion by half as compared to control. In addition, the miR29b significantly improved post-stroke sensorimotor functions, where the cohort receiving miR29b has better agility and movement 48 hours post stroke, compared to control.
Prof. Sen went on to test the efficacy of alpha-tocotrienol in the same mouse stroke model. Test mice given 50mg/kg body weight of alpha-tocotrienol (from Tocomin, Carotech Inc.) and control mice given vitamin-E stripped corn oil for 10 weeks before subjecting them to MCAO. The result showed that stroke-induced loss of miR29b was completely spared in the tocotrienol supplemented group, which resulted in smaller lesion size.
“I am excited with this new 5th checkpoint of tocotrienol in preventing stroke-induced injuries. It further strengthens the science of Tocomin for neuroprotection. In a stroke event, neuroprotective miR29b is loss due to the downstream product of 12-Lipoxygenase (12-Lox) called 12HETE, which leads to neuronal cell death. Tocomin is able to rescue miR29b by inhibiting 12-Lox,” said Mr. WH Leong, vice president of Carotech Inc.
“The findings from this latest NIH-funded study are unprecedented and provided further evidence to the unique neuroprotective benefit of TocominNatural Full Spectrum Palm Tocotrienol Complex. Carotech is proud to collaborate with OSU Wexner Medical Center and be part of this amazing discovery,” added Mr. Leong.
For more information: www.carotech.net
In the study, Professor Chandan K. Sen and his team of researchers at The Ohio State University Wexner Medical Center, Columbus, USA, elucidated the mechanisms of microRNA precursor (miR29) in stroke-induced neuronal injuries. They showed that alpha-tocotrienol (Tocomin, Carotech Inc.) prevented miR29 loss at the infarct site during stroke and therefore protected the neurons from cell death (apoptosis).
“Micro RNAs (miR) are small non-coding RNA molecules that play important role in regulating gene expression at the translation level, and miR29 is the micro RNA in the study of stroke etiology and in many other neurodegenerative disorders including Alzheimer’s Disease,” said Dr. Savita Khanna, co-researcher of the study, at the recently concluded Palm International Nutraceutical Conference at Kuala Lumpur.
The miR29 family of genes - miR29a, miR29b1, miR29b2 (collectively miR29b) and miR29c in the human genome plays an important role in regulating gene expression. MiR29b isrecognized as a neuronal survival factor. Specific loss of miR-29b at the infarct site after stroke leads to neuronal cell death. As such, prevention of such stroke-induced loss of miR-29b significantly improves stroke outcomes.
The researchers used the mouse stroke model, where mice were subjected to temporary middle-cerebral artery occlusion (MCAO) to induce stroke. At 48 hours after MCAO, there was a significant loss of miR29b at the infarct site.
By re-introducing miR29b at the infarct site, it decreased stroke-induced brain lesion by half as compared to control. In addition, the miR29b significantly improved post-stroke sensorimotor functions, where the cohort receiving miR29b has better agility and movement 48 hours post stroke, compared to control.
Prof. Sen went on to test the efficacy of alpha-tocotrienol in the same mouse stroke model. Test mice given 50mg/kg body weight of alpha-tocotrienol (from Tocomin, Carotech Inc.) and control mice given vitamin-E stripped corn oil for 10 weeks before subjecting them to MCAO. The result showed that stroke-induced loss of miR29b was completely spared in the tocotrienol supplemented group, which resulted in smaller lesion size.
“I am excited with this new 5th checkpoint of tocotrienol in preventing stroke-induced injuries. It further strengthens the science of Tocomin for neuroprotection. In a stroke event, neuroprotective miR29b is loss due to the downstream product of 12-Lipoxygenase (12-Lox) called 12HETE, which leads to neuronal cell death. Tocomin is able to rescue miR29b by inhibiting 12-Lox,” said Mr. WH Leong, vice president of Carotech Inc.
“The findings from this latest NIH-funded study are unprecedented and provided further evidence to the unique neuroprotective benefit of TocominNatural Full Spectrum Palm Tocotrienol Complex. Carotech is proud to collaborate with OSU Wexner Medical Center and be part of this amazing discovery,” added Mr. Leong.
For more information: www.carotech.net
