Polygalae Radix,which has a long history of medical use in traditional Chinese medicine,is multifunctional such as tranquilize mind,relieve swelling and remove phlegm.It has been demonstrated that Polygalae Radix olig...Polygalae Radix,which has a long history of medical use in traditional Chinese medicine,is multifunctional such as tranquilize mind,relieve swelling and remove phlegm.It has been demonstrated that Polygalae Radix oligosaccharide ester is the main active component which excutes the neuropharmacological activities like antidepression,anti-dementia and neuroprotection.In this review,the chemical structure,pharmacology,pharmacokinetics and processing mechanism of Polygalae Radix oligosaccharide ester are summarized so as to provide reference for its further development and utilization.展开更多
OBJECTIVE To investigate the autophagic effect of the compounds from the Chinese medicinal herbs,Radix polygalae as a potential neuroprotective agent that enhances the clearance of mutant Huntingtin andα-synuclein in...OBJECTIVE To investigate the autophagic effect of the compounds from the Chinese medicinal herbs,Radix polygalae as a potential neuroprotective agent that enhances the clearance of mutant Huntingtin andα-synuclein in PC-12 cells.METHODS Radix polygalae was extracted with 75%ethanol using refluxing method,and its quality was assayed by UHPLC-TOF-MS.The autophagic effect of Radix polygalae extract,and its major components including polygalacic acid,senegenin and onjisaponin B were investigated using the green fluorescent protein-light chain 3(GFP-LC3)autophagy detection and Western blot platforms for detecting the autophagic markers,GFP-LC3 puncta formation and LC3Ⅱ expression.The degradation of A53Tα-synuclein and the inhibition of α-synuclein oligo merization related to the Parkinson disease were assayed using Western blot and flow cytometer analysis,respectively.While the cytotoxicity and the degradation of the mutant Huntingtin associated with the Huntingtin disease were investigated using MTT method and flow cytometer analysis.RESULTS Radix polygalae ethanol extract and onjisaponin B improved the GFP-LC3 puncta formation and expression of LC3Ⅱ with time and dose manner,and this induction was activated via AMPK-m TOR and Atg 7 gene pathway.Furthermore,the clearance ofα-synuclein and mutant Huntingtin was enhanced via autophagy induction with the treatment of Radix polygalae ethanol extract and onjisaponin B.CONCLUSION Findings in the current study provide detailed insights into the protective mechanism of a novel autophagy inducer,onjisaponin B,which is valuable for further investigation as a new candidate agent for modulating neurodegenerative disorders through the reduction of toxicity and clearance of mutant proteins in the cellular level.展开更多
Kai Xin San is a Chinese herbal formula composed of Radix Ginseng, Poria, Radix Polygalae and Acorus Tatarinowii Rhizome. It has been used in China for many years for treating amnesia. Kai Xin San ameliorates amyloid-...Kai Xin San is a Chinese herbal formula composed of Radix Ginseng, Poria, Radix Polygalae and Acorus Tatarinowii Rhizome. It has been used in China for many years for treating amnesia. Kai Xin San ameliorates amyloid-β(Aβ)-induced cognitive dysfunction and is neuroprotective in vivo, but its precise mechanism remains unclear. Expression of insulin-degrading enzyme(IDE), which degrades Aβ, is strongly correlated with cognitive function. Here, we injected rats with exogenous Aβ42(200 μM, 5 μL) into the hippocampus and subsequently administered Kai Xin San(0.54 or 1.08 g/kg/d) intragastrically for 21 consecutive days. Hematoxylin-eosin and Nissl staining revealed that Kai Xin San protected neurons against Aβ-induced damage. Furthermore, enzyme-linked immunosorbent assay, western blot and polymerase chain reaction results showed that Kai Xin San decreased Aβ42 protein levels and increased expression of IDE protein, but not m RNA, in the hippocampus. Our findings reveal that Kai Xin San facilitates hippocampal Aβ degradation and increases IDE expression, which leads, at least in part, to the alleviation of hippocampal neuron injury in rats.展开更多
文摘Polygalae Radix,which has a long history of medical use in traditional Chinese medicine,is multifunctional such as tranquilize mind,relieve swelling and remove phlegm.It has been demonstrated that Polygalae Radix oligosaccharide ester is the main active component which excutes the neuropharmacological activities like antidepression,anti-dementia and neuroprotection.In this review,the chemical structure,pharmacology,pharmacokinetics and processing mechanism of Polygalae Radix oligosaccharide ester are summarized so as to provide reference for its further development and utilization.
基金supported by Macao Foundation(Project code:0212)FDCT grant from the Science and Technology Development Fund of Macao(Project code:076/2011/A3)
文摘OBJECTIVE To investigate the autophagic effect of the compounds from the Chinese medicinal herbs,Radix polygalae as a potential neuroprotective agent that enhances the clearance of mutant Huntingtin andα-synuclein in PC-12 cells.METHODS Radix polygalae was extracted with 75%ethanol using refluxing method,and its quality was assayed by UHPLC-TOF-MS.The autophagic effect of Radix polygalae extract,and its major components including polygalacic acid,senegenin and onjisaponin B were investigated using the green fluorescent protein-light chain 3(GFP-LC3)autophagy detection and Western blot platforms for detecting the autophagic markers,GFP-LC3 puncta formation and LC3Ⅱ expression.The degradation of A53Tα-synuclein and the inhibition of α-synuclein oligo merization related to the Parkinson disease were assayed using Western blot and flow cytometer analysis,respectively.While the cytotoxicity and the degradation of the mutant Huntingtin associated with the Huntingtin disease were investigated using MTT method and flow cytometer analysis.RESULTS Radix polygalae ethanol extract and onjisaponin B improved the GFP-LC3 puncta formation and expression of LC3Ⅱ with time and dose manner,and this induction was activated via AMPK-m TOR and Atg 7 gene pathway.Furthermore,the clearance ofα-synuclein and mutant Huntingtin was enhanced via autophagy induction with the treatment of Radix polygalae ethanol extract and onjisaponin B.CONCLUSION Findings in the current study provide detailed insights into the protective mechanism of a novel autophagy inducer,onjisaponin B,which is valuable for further investigation as a new candidate agent for modulating neurodegenerative disorders through the reduction of toxicity and clearance of mutant proteins in the cellular level.
基金supported by the National Natural Science Foundation of China,No.81303248,81603321the Natural Science Foundation of Heilongjiang Province of China,No.H2015028+1 种基金a grant from the Nursing Program for Young Scholars of Heilongjiang Province of China,No.UNPYSCT-2016116the Scientific Research Fund for Doctors of Qiqihar Medical University in China,No.QY2016B-09
文摘Kai Xin San is a Chinese herbal formula composed of Radix Ginseng, Poria, Radix Polygalae and Acorus Tatarinowii Rhizome. It has been used in China for many years for treating amnesia. Kai Xin San ameliorates amyloid-β(Aβ)-induced cognitive dysfunction and is neuroprotective in vivo, but its precise mechanism remains unclear. Expression of insulin-degrading enzyme(IDE), which degrades Aβ, is strongly correlated with cognitive function. Here, we injected rats with exogenous Aβ42(200 μM, 5 μL) into the hippocampus and subsequently administered Kai Xin San(0.54 or 1.08 g/kg/d) intragastrically for 21 consecutive days. Hematoxylin-eosin and Nissl staining revealed that Kai Xin San protected neurons against Aβ-induced damage. Furthermore, enzyme-linked immunosorbent assay, western blot and polymerase chain reaction results showed that Kai Xin San decreased Aβ42 protein levels and increased expression of IDE protein, but not m RNA, in the hippocampus. Our findings reveal that Kai Xin San facilitates hippocampal Aβ degradation and increases IDE expression, which leads, at least in part, to the alleviation of hippocampal neuron injury in rats.
