An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

Background and Objectives: Angiographic assessment of coronary stenosis severity using quantitative coronary angiography (QCA) is often inconsistent with that based on fractional flow reserve (FFR) or intravascular ultrasound (IVUS). We investigated the incidence of discrepancies between QCA and FFR or IVUS, and the outcomes of FFR- and IVUS-guided strategies in discordant coronary lesions. Methods: This study was a post-hoc analysis of the FLAVOUR study. We used a QCA-derived diameter stenosis (DS) of 60% or greater, the highest tertile, to classify coronary lesions as concordant or discordant with FFR or IVUS criteria for percutaneous coronary intervention (PCI). The patient-oriented composite outcome (POCO) was defined as a composite of death, myocardial infarction, or revascularization at 24 months. Results: The discordance rate between QCA and FFR or IVUS was 30.2% (n=551). The QCAFFR discordance rate was numerically lower than the QCA-IVUS discordance rate (28.2% vs. 32.4%, p=0.050). In 200 patients with ≥60% DS, PCI was deferred according to negative FFR (n=141) and negative IVUS (n=59) (15.3% vs. 6.5%, p<0.001). The POCO incidence was comparable between the FFR- and IVUS-guided deferral strategies (5.9% vs. 3.4%, p=0.479).Conversely, 351 patients with DS <60% underwent PCI according to positive FFR (n=118) and positive IVUS (n=233) (12.8% vs. 25.9%, p<0.001). FFR- and IVUS-guided PCI did not differ in the incidence of POCO (9.5% vs. 6.5%, p=0.294). Conclusions The proportion of QCA-FFR or IVUS discordance was approximately one third for intermediate coronary lesions. FFR- or IVUS-guided strategies for these lesions were comparable with respect to POCO at 24 months.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

Background and Objectives: Angiographic assessment of coronary stenosis severity using quantitative coronary angiography (QCA) is often inconsistent with that based on fractional flow reserve (FFR) or intravascular ultrasound (IVUS). We investigated the incidence of discrepancies between QCA and FFR or IVUS, and the outcomes of FFR- and IVUS-guided strategies in discordant coronary lesions. Methods: This study was a post-hoc analysis of the FLAVOUR study. We used a QCA-derived diameter stenosis (DS) of 60% or greater, the highest tertile, to classify coronary lesions as concordant or discordant with FFR or IVUS criteria for percutaneous coronary intervention (PCI). The patient-oriented composite outcome (POCO) was defined as a composite of death, myocardial infarction, or revascularization at 24 months. Results: The discordance rate between QCA and FFR or IVUS was 30.2% (n=551). The QCAFFR discordance rate was numerically lower than the QCA-IVUS discordance rate (28.2% vs. 32.4%, p=0.050). In 200 patients with ≥60% DS, PCI was deferred according to negative FFR (n=141) and negative IVUS (n=59) (15.3% vs. 6.5%, p<0.001). The POCO incidence was comparable between the FFR- and IVUS-guided deferral strategies (5.9% vs. 3.4%, p=0.479).Conversely, 351 patients with DS <60% underwent PCI according to positive FFR (n=118) and positive IVUS (n=233) (12.8% vs. 25.9%, p<0.001). FFR- and IVUS-guided PCI did not differ in the incidence of POCO (9.5% vs. 6.5%, p=0.294). Conclusions The proportion of QCA-FFR or IVUS discordance was approximately one third for intermediate coronary lesions. FFR- or IVUS-guided strategies for these lesions were comparable with respect to POCO at 24 months.

Background and Objectives: Angiographic assessment of coronary stenosis severity using quantitative coronary angiography (QCA) is often inconsistent with that based on fractional flow reserve (FFR) or intravascular ultrasound (IVUS). We investigated the incidence of discrepancies between QCA and FFR or IVUS, and the outcomes of FFR- and IVUS-guided strategies in discordant coronary lesions. Methods: This study was a post-hoc analysis of the FLAVOUR study. We used a QCA-derived diameter stenosis (DS) of 60% or greater, the highest tertile, to classify coronary lesions as concordant or discordant with FFR or IVUS criteria for percutaneous coronary intervention (PCI). The patient-oriented composite outcome (POCO) was defined as a composite of death, myocardial infarction, or revascularization at 24 months. Results: The discordance rate between QCA and FFR or IVUS was 30.2% (n=551). The QCAFFR discordance rate was numerically lower than the QCA-IVUS discordance rate (28.2% vs. 32.4%, p=0.050). In 200 patients with ≥60% DS, PCI was deferred according to negative FFR (n=141) and negative IVUS (n=59) (15.3% vs. 6.5%, p<0.001). The POCO incidence was comparable between the FFR- and IVUS-guided deferral strategies (5.9% vs. 3.4%, p=0.479).Conversely, 351 patients with DS <60% underwent PCI according to positive FFR (n=118) and positive IVUS (n=233) (12.8% vs. 25.9%, p<0.001). FFR- and IVUS-guided PCI did not differ in the incidence of POCO (9.5% vs. 6.5%, p=0.294). Conclusions The proportion of QCA-FFR or IVUS discordance was approximately one third for intermediate coronary lesions. FFR- or IVUS-guided strategies for these lesions were comparable with respect to POCO at 24 months.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

Background and Objectives: Angiographic assessment of coronary stenosis severity using quantitative coronary angiography (QCA) is often inconsistent with that based on fractional flow reserve (FFR) or intravascular ultrasound (IVUS). We investigated the incidence of discrepancies between QCA and FFR or IVUS, and the outcomes of FFR- and IVUS-guided strategies in discordant coronary lesions. Methods: This study was a post-hoc analysis of the FLAVOUR study. We used a QCA-derived diameter stenosis (DS) of 60% or greater, the highest tertile, to classify coronary lesions as concordant or discordant with FFR or IVUS criteria for percutaneous coronary intervention (PCI). The patient-oriented composite outcome (POCO) was defined as a composite of death, myocardial infarction, or revascularization at 24 months. Results: The discordance rate between QCA and FFR or IVUS was 30.2% (n=551). The QCAFFR discordance rate was numerically lower than the QCA-IVUS discordance rate (28.2% vs. 32.4%, p=0.050). In 200 patients with ≥60% DS, PCI was deferred according to negative FFR (n=141) and negative IVUS (n=59) (15.3% vs. 6.5%, p<0.001). The POCO incidence was comparable between the FFR- and IVUS-guided deferral strategies (5.9% vs. 3.4%, p=0.479).Conversely, 351 patients with DS <60% underwent PCI according to positive FFR (n=118) and positive IVUS (n=233) (12.8% vs. 25.9%, p<0.001). FFR- and IVUS-guided PCI did not differ in the incidence of POCO (9.5% vs. 6.5%, p=0.294). Conclusions The proportion of QCA-FFR or IVUS discordance was approximately one third for intermediate coronary lesions. FFR- or IVUS-guided strategies for these lesions were comparable with respect to POCO at 24 months.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

BACKGROUND/OBJECTIVES: There is growing interest in herbal medicines for managing age-related diseases, such as Alzheimer's and Parkinson’s. Safflower seeds (Carthamus tinctorius L. seeds, CTS) and dandelions (Taraxacum coreanum, TC) are widely used to treat bone- or inflammation-related diseases in Oriental countries. This study investigated the protective effect of the CTS–TC combination on scopolamine (Sco)-induced memory deficits through inflammatory response and cholinergic function. Moreover, marker components such as serotonin, N-(p-coumaroyl) serotonin, N-feruloylserotonin, chlorogenic acid, and chicoric acid in the CTS–TC combination were analyzed for their potential benefits on memory function.MATERIALS/METHODS: Water extracts of CTS, TC, and the CTS–TC combination at various ratios (4:1, 1:1, and 1:4) (100 mg/kg) were orally administered to mice for 14 days. Sco (1 mg/kg) was intraperitoneally injected into the mice before each behavioral test. T-maze and novel object recognition tests were conducted to monitor behavioral changes after the treatment.Western blotting was performed to detect protein expression. In addition, the presence of 5 biomarkers, serotonin, N-(p-coumaroyl) serotonin, N-feruloylserotonin, chlorogenic acid, and chicoric acid, was analyzed using high-performance liquid chromatography (HPLC). RESULTS: Behavioral tests showed that the CTS–TC combination enhanced memory function in Sco-injected mice. Inflammation-related proteins (inducible nitric oxide synthase, cyclooxygenase-2, and glial fibrillary acidic protein) were downregulated after treatment with the CTS–TC combination. The acetylcholinesterase protein expression was also downregulated.HPLC analysis revealed that N-feruloylserotonin and chicoric acid were the predominant components, followed by N-(p-coumaroyl) serotonin, chlorogenic acid, and serotonin. CONCLUSION These findings suggest that the CTS–TC combination protects against Sco-induced memory deficits by inhibiting inflammatory responses and cholinergic dysfunction. N-feruloylserotonin and chicoric acid, along with N-(p-coumaroyl) serotonin, chlorogenic acid, and serotonin, might be biomarkers for the CTS–TC combination, and their effects on memory protection warrant further study.