• Title/Summary/Keyword: Materia medica

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Foeniculum vulgare essential oil nanoemulsion inhibits Fusarium oxysporum causing Panax notoginseng root-rot disease

  • Hongyan Nie;Hongxin Liao;Jinrui Wen;Cuiqiong Ling;Liyan Zhang;Furong Xu;Xian Dong
    • Journal of Ginseng Research
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    • v.48 no.2
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    • pp.236-244
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    • 2024
  • Background: Fusarium oxysporum (F. oxysporum) is the primary pathogenic fungus that causes Panax notoginseng (P. notoginseng) root rot disease. To control the disease, safe and efficient antifungal pesticides must currently be developed. Methods: In this study, we prepared and characterized a nanoemulsion of Foeniculum vulgare essential oil (Ne-FvEO) using ultrasonic technology and evaluated its stability. Traditional Foeniculum vulgare essential oil (T-FvEO) was prepared simultaneously with 1/1000 Tween-80 and 20/1000 dimethyl sulfoxide (DMSO). The effects and inhibitory mechanism of Ne-FvEO and T-FvEO in F. oxysporum were investigated through combined transcriptome and metabolome analyses. Results: Results showed that the minimum inhibitory concentration (MIC) of Ne-FvEO decreased from 3.65 mg/mL to 0.35 mg/mL, and its bioavailability increased by 10-fold. The results of gas chromatography/mass spectrometry (GC/MS) showed that T-FvEO did not contain a high content of estragole compared to Foeniculum vulgare essential oil (FvEO) and Ne-FvEO. Combined metabolome and transcriptome analysis showed that both emulsions inhibited the growth and development of F. oxysporum through the synthesis of the cell wall and cell membrane, energy metabolism, and genetic information of F. oxysporum mycelium. Ne-FvEO also inhibited the expression of 2-oxoglutarate dehydrogenase and isocitrate dehydrogenase and reduced the content of 2-oxoglutarate, which inhibited the germination of spores. Conclusion: Our findings suggest that Ne-FvEO effectively inhibited the growth of F. oxysporum in P. notoginseng in vivo. The findings contribute to our comprehension of the antifungal mechanism of essential oils (EOs) and lay the groundwork for the creation of plant-derived antifungal medicines.

Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissue

  • Chen, Weijie;Wang, Junlian;Luo, Yong;Wang, Tao;Li, Xiaochun;Li, Aiyun;Li, Jia;Liu, Kang;Liu, Baolin
    • Journal of Ginseng Research
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    • v.40 no.4
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    • pp.351-358
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    • 2016
  • Background: This study was designed to investigate whether ginsenoside Rb1 (Rb1) and compound K (CK) ameliorated insulin resistance by suppressing endoplasmic reticulum (ER) stress-induced inflammation in adipose tissue. Methods: To induce ER stress, epididymal adipose tissue from mice or differentiated 3T3 adipocytes were exposed to high glucose. The effects of Rb1 and CK on reactive oxygen species production, ER stress, TXNIP/NLRP3 inflammasome activation, inflammation, insulin signaling activation, and glucose uptake were detected by western blot, emzyme-linked immunosorbent assay, or fluorometry. Results: Rb1 and CK suppressed ER stress by dephosphorylation of $IRE1{\alpha}$ and PERK, thereby reducing TXNIP-associated NLRP3 inflammasome activation in adipose tissue. As a result, Rb1 and CK inhibited IL-$1{\beta}$ maturation and downstream inflammatory factor IL-6 secretion. Inflammatory molecules induced insulin resistance by upregulating phosphorylation of insulin receptor substrate-1 at serine residues and impairing insulin PI3K/Akt signaling, leading to decreased glucose uptake by adipocytes. Rb1 and CK reversed these changes by inhibiting ER stress-induced inflammation and ameliorating insulin resistance, thereby improving the insulin IRS-1/PI3K/Akt-signaling pathway in adipose tissue. Conclusion: Rb1 and CK inhibited inflammation and improved insulin signaling in adipose tissue by suppressing ER stress-associated NLRP3 inflammation activation. These findings offered novel insight into the mechanism by which Rb1 and CK ameliorate insulin resistance in adipose tissue.

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
    • Journal of Ginseng Research
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    • v.39 no.2
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    • pp.116-124
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    • 2015
  • 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.

Studies on the Hypoglycemic Effect of Ginseng Polypeptide

  • Wang, B.X;Yang, M.;Jin, Y.L.;Cui, X.Y.;Wang, Y.
    • Proceedings of the Ginseng society Conference
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    • 1990.06a
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    • pp.196-200
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    • 1990
  • the ginseng polypeptide (GPP) isolated from the root of Panax ginseng C.A. Meyer was demonstrated to decrease the levels of blood sugar and hepatic glycogen when injected intravenously to rats at a doses of 50-200mg/kg without affecting blood total lipid. When mice were injected subcutaneously daily at a dose of 50 and 100mg/kg for 7 successive days, GPP was also found to decreased blood sugar and hepatic glycoge. In addition, GPP was found to decrease various experimenta hyperglycemias induced by injection of adrenaline, glucose and alloxan. GPP exhibited inhibiting effect on the glycogen enhancement induced by glucose, but strengthening effect on the glycogen decrease induced by adrenaline. When the levels of blood total lipid and liver glycogen were increased by alloxan, GPP was shown to inhibit these changes except its lowering blood sugar. the toxicity of GPP is very low, its LD50 was found to be 1.62$\pm$0.130 g/kg for iv.

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Studies on the Hypoglycemic Effect of ginseng Polypeptide (인삼의 폴리펩티드 성분의 혈당저하에 미치는 영향)

  • Wang, B.X.;Yang, M.;Jin, Y.L.;Cui, X.Y.;Wang, Y.
    • Journal of Ginseng Research
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    • v.14 no.2
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    • pp.338-342
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    • 1990
  • The ginseng Polypeptide (GPP) Isolated from the root of Panax ginseng C.A. Meyer was domonstrated to decrease the levels of blood sugar and hepatic glycogen when injected intravenoilsly to rats at a doses of 50-200 mg/kg without affecting blood total lipid. When mice were injected slibclitaneollsly daily at a dose of 50 and 100 mg/kg for 7 successive days. GPP was also found to decrease blood sligar and hepatic glycogen. In addition, GPP was found to decrease variolls experimental hypergly cemias induced by injection of adrenaline, glilcose and alloxan. GPP exhibited inhibiting effect on the glut rogen enhancement indllced by glucose, but strenthening effect on the glycogen decrease indliced by adrenaline. When the levels of blood total lipid and lilrer glycogen were increased by T alloxan. GPP was shown to inhibit these changes except its lowering blood sugar. The toxicity of GPP is very low, LD50 was found to be 1.62 $\pm$ 0.130 g/kg for iv.

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Bioactive Natural Products from Chinese Tropical Marine Plants and Invertebrates

  • Guo, Y.W.;Huang, X.C.;Zhang, W.;Sun, Y.Q.
    • Journal of Marine Bioscience and Biotechnology
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    • v.1 no.1
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    • pp.22-33
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    • 2006
  • This paper deals mainly with chemical and biological investigations, recently effected in the authors' laboratory, of Chinese tropical marine plants and invertebrates on three topics: 1) an unusual macrocyclic polydisulfide from the Chinese mangrove Bruguiera gymnorrhiza; 2) polyhydroxylpolyene compounds from marine dinoflagellate Amphidinium sp.; 3) two new series of uncommon steroids from marine in vertebrates.

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A Review on the Food-Therapy with Five-Grain in 『Sikryochanyo』 (『식료찬요(食療纂要)』에서 오곡(五穀)을 이용한 식치(食治) 연구(硏究))

  • Yoon, Seo-Hyun;Lee, Seong-Jin;Jo, Eun-Hee;Song, Ji-Chung
    • The Journal of Korean Medical History
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    • v.24 no.2
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    • pp.105-116
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    • 2011
  • Objective : Foods could be materia medica through food-therapy in oriental medicine. "Sikryochanyo" is a food-therapy book totally. Therefore, there are many kinds of food are treated as materia medica. Method : Finding out cases of food-therapy with Five-Grain(RIce, Barley, Millet, Soy, Panicum miliaceum) in "Sikryochanyo" Result : In "Sikryochanyo", there were many methods of food-therapy with Five-Grain. Five-Grain were treated as materia medica even though they were usual food as normal meal. Conclusion : Five-Grain used in "Sikryochanyo" as many types of themselves and they had objectively effects comparing with "Materia Medica".

Alkaloid from Stemona and Lyophyllum

  • Yang Ye;Lin, Wen-han;Qin, Guo-wei;Xu, Ren-sheng;Wu, Hou-ming;Yi Zhong;Zhong, Qiong-xing;Wolfgang Steglich
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1998.11a
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    • pp.62-65
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    • 1998
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