Ginseng improves cognitive deficit via the RAGE/NF-kB pathway in advanced glycation end product-induced rats

Xiaobin Tan,Junfei Gu,Bingjie Zhao,Shuyuan Wang,Jiarui Yuan,Chunfei Wang,Juan Chen,Jiping Liu,Liang Feng,Xiaobin Jia 고려인삼학회 2015 Journal of Ginseng Research Vol.39 No.2

Background: Ginseng, the root of Panax ginseng (PG), is used widely as a herbal medicine to prevent andtreat various diseases. Panax ginseng has pharmacological effects on neurodegenerative diseases such asAlzheimer’s disease (AD). The present study evaluated the neuroprotective effects of PG and its possibleneuroprotective mechanisms in advanced glycation end product (AGE)-induced AD in a rat model. Methods: Advanced glycation end products were injected bilaterally into the CA3 region of the rats’brains. The Morris water maze test and step-down type passive avoidance test were performed toevaluate their memory and cognitive abilities. The oxidation indexes in the hippocampus were detected. Immunohistochemistry was conducted to visualize the receptors for advanced glycation end products(RAGEs) and nuclear factor-kappa-light-chain-enhancer of activated B cell (NF-kB). Results: Behavioral results showed that PG (1 g/kg, 0.5 g/kg, and 0.25 g/kg) significantly shortened theescape latency, remarkably increased the number of crossing times, significantly decreased the numberof errors, and prolonged the latency in rats with AGE-induced AD. Panax ginseng also significantlyreduced the malondialdehyde level, increased the glutathione content, and increased superoxide dismutaseactivity in the hippocampus. Panax ginseng significantly decreased the expression of RAGE andNF-kB. The blockade of anti-RAGE antibody could significantly reduce AGE-induced impairments andregulate these expressions. Conclusion: Our results demonstrated that PG significantly inhibits AGE-induced memory impairmentand attenuates Alzheimer-like pathophysiological changes. These neuroprotective effects of PG may beassociated with the RAGE/NF-kB pathway. Our results provided the experimental basis for applying PG inpreventing and treating AD.

Ginseng improves cognitive deficit via the RAGE/NF-κB pathway in advanced glycation end product-induced rats

Tan, Xiaobin,Gu, Junfei,Zhao, Bingjie,Wang, Shuyuan,Yuan, Jiarui,Wang, Chunfei,Chen, Juan,Liu, Jiping,Feng, Liang,Jia, Xiaobin The Korean Society of Ginseng 2015 Journal of Ginseng Research Vol.39 No.2

Background: Ginseng, the root of Panax ginseng (PG), is used widely as a herbal medicine to prevent and treat various diseases. Panax ginseng has pharmacological effects on neurodegenerative diseases such as Alzheimer's disease (AD). The present study evaluated the neuroprotective effects of PG and its possible neuroprotective mechanisms in advanced glycation end product (AGE)-induced AD in a rat model. Methods: Advanced glycation end products were injected bilaterally into the CA3 region of the rats' brains. The Morris water maze test and step-down type passive avoidance test were performed to evaluate their memory and cognitive abilities. The oxidation indexes in the hippocampus were detected. Immunohistochemistry was conducted to visualize the receptors for advanced glycation end products (RAGEs) and nuclear factor-kappa-light-chain-enhancer of activated B cell (NF-${\kappa}B$). Results: Behavioral results showed that PG (1 g/kg, 0.5 g/kg, and 0.25 g/kg) significantly shortened the escape latency, remarkably increased the number of crossing times, significantly decreased the number of errors, and prolonged the latency in rats with AGE-induced AD. Panax ginseng also significantly reduced the malondialdehyde level, increased the glutathione content, and increased superoxide dismutase activity in the hippocampus. Panax ginseng significantly decreased the expression of RAGE and NF-${\kappa}B$. The blockade of anti-RAGE antibody could significantly reduce AGE-induced impairments and regulate these expressions. Conclusion: Our results demonstrated that PG significantly inhibits AGE-induced memory impairment and attenuates Alzheimer-like pathophysiological changes. These neuroprotective effects of PG may be associated with the RAGE/NF-${\kappa}B$ pathway. Our results provided the experimental basis for applying PG in preventing and treating AD.

Experimental Research on Double-walled Carbon Nanotubes by Using Tip-enhanced Raman Spectroscopy

Mingqian Zhang,,Xiaobin Wu,Jia Wang,Qian Tian 한국물리학회 2010 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.56 No.4

In this research, a transmission mode tip-enhanced Raman spectroscopy (TERS) system is set up. Using this self-made TERS system, topographic images and corresponding TERS spectra of positions of interest on a thin film of dispersed double-walled carbon nanotubes (DWNTs) are investigated. The Raman enhancement factor is estimated to be 3.6 × 102. TERS spectra of different measured positions show distinct Raman features that represent their different components and structures. This indicates that characterization of DWNTs and Raman spectral recognition can be realized. The experimental results indicate that there is a peak shift between the TERS and the far-field spectrum in radial breathing mode region, which may be attributed to a combination of the tip’s mechanical pressure and the interaction between the two layer tube walls of the DWNTs.

Metabolite profiles of ginsenosides Rk1 and Rg5 in zebrafish using ultraperformance liquid chromatography/quadrupole-time-of-flight MS

Shen, Wenwen,Wei, Yingjie,Tang, Daoquan,Jia, Xiaobin,Chen, Bin The Korean Society of Ginseng 2017 Journal of Ginseng Research Vol.41 No.1

Background: In the present study, metabolite profiles of ginsenosides Rk1 and Rg5 from red ginseng or red notoginseng in zebrafish were qualitatively analyzed with ultraperformance liquid chromatography/quadrupole-time-of-flight MS, and the possible metabolic were pathways proposed. Methods: After exposing to zebrafish for 24 h, we determined the metabolites of ginsenosides Rk1 and Rg5. The chromatography was accomplished on UPLC BEH C18 column using a binary gradient elution of 0.1% formic acetonitrile-0.1% formic acid water. The quasimolecular ions of compounds were analyzed in the negative mode. With reference to quasimolecular ions and MS2 spectra, by comparing with reference standards and matching the empirical molecular formula with that of known published compounds, and then the potential structures of metabolites of ginsenosides Rk1 and Rg5 were acquired. Results: Four and seven metabolites of ginsenoside Rk1 and ginsenoside Rg5, respectively, were identified in zebrafish. The mechanisms involved were further deduced to be desugarization, glucuronidation, sulfation, and dehydroxymethylation pathways. Dehydroxylation and loss of C-17 residue were also metabolic pathways of ginsenoside Rg5 in zebrafish. Conclusion: Loss of glucose at position C-3 and glucuronidation at position C-12 in zebrafish were regarded as the primary physiological processes of ginsenosides Rk1 and Rg5.

Metabolism of ginsenosides Rk3 and Rh4 from steamed notoginseng in zebrafish by ultraperformance liquid chromatography/quadrupole-time-of-flight mass spectrometry

Bin Chen,Yingjie Wei,Dandan Wang,Xiaobin Jia 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.8

In this work, the metabolite profiles of ginsenosides Rk3 and Rh4 from steamed notoginseng in zebrafish were qualitatively investigated, and their possible metabolic pathways were subsequently proposed. Metabolites of ginsenosides Rk3 and Rh4 after exposing to zebrafish for 24 h were identified by Ultraperformance Liquid Chromatography/Quadrupole -Time-of-Flight Mass Spectrometry (UPLC-TOF/MS). The separation was performed with a UPLC BEH C18 column using a binary gradient elution of 0.1 % formic acetonitrile -0.1 % formic acid water. The quasi-molecular ions of compounds were detected in negative mode. According to the quasi-molecular ions and MS2 spectra, after comparison with reference standards, molecular mass information and the potential structures about metabolites of ginsenosides Rk3 and Rh4 were obtained. In all, 5 and 6 metabolites of ginsenoside Rk3 and Rh4 including M1(M6), M2(M7), M3–M5 and N1, N2(N7), N3–N6 were identified in zebrafish respectively, which were to our knowledge reported for the first time. The results indicated that ginsenosides Rk3 and Rh4 were metabolized via desugarization, glucuronidation, sulfation, dehydroxylation, and loss of C-17 and C-23 residue pathways in zebrafish. Loss of glucose at position C-6 and glucuronidation at position C-3 or C-6 in zebrafish were considered as the main physiologic processes of ginsenosides Rk3 and Rh4.

Hypoglycemic and Antioxidant Activities of Paeonol and Its Beneficial Effect on Diabetic Encephalopathy in Streptozotocin-Induced Diabetic Rats

Jiping Liu,Shuyuan Wang,Liang Feng,Dongying Ma,Qiang Fu,Yu Song,Xiaobin Jia,Shiping Ma 한국식품영양과학회 2013 Journal of medicinal food Vol.16 No.7

Diabetic encephalopathy (DE) is one of the severe complications in patients with diabetes mellitus. Paeonol, an active compound isolated from the root bark of Paeonia suffruticosa, has significant antidiabetic activity in vivo. However, its underlying beneficial effects on DE were unclear. In the present study, the protective activity of paeonol on DE was evaluated in streptozotocin (STZ)-induced diabetic rats. Paeonol at 50 and 100mg/kg significantly increased body weight and decreased blood glucose levels, glycosylated serum proteins, and serum advanced glycation end products (AGEs) levels. Immunohistochemistry assays and Western blot analysis revealed a significant decrease in expressions on receptor for advanced glycation end products (RAGE) and nuclear factor kappa B (NF-jB) in hippocampus and cerebral cortical neurons after paeonol treatment. Furthermore, paeonol significantly increased glutathione content and remarkedly decreased induced nitric oxide synthase activity in hippocampus tissue. Our findings indicated that paeonol could improve the pathological damage of DE in STZ-induced diabetic rats. It might be associated with the modulating AGEs/RAGE/NF-jB pathway. This study suggested that paeonol might be a promising candidate for the prevention and treatment of DE.