This experiment was conducted to investigate the effect of deep sea water on fruit quality and yield of tomato. In the deep sea water treatments, fruit growth and weight were decreased as the concentration of deep sea water increased. Especially, the fresh weight of second truss was decreased significantly than first truss. Soluble solid content was increased significantly in higher concentration treatment especially at 30mM and 40mM treatment. That was increased more in the first than in the second truss fruits. Most of hexose in fruits were glucose and fructose. The reason of increased glucose and fructose contents was the decline of growth because of salinity stress by deep sea water treatment. however deep sea water treatment increased the lycopene content, especially in 20mM treatment. It is assumed that deep sea water treatment cause induction and promotion of ethylene. The higher concentration of deep sea water to the solution, the eater fruit quality improvement was noticed. However, proportional yield reduction accompanied concentration, 20mM deep sea water improved fruit quality without a significant yield reduction. The Re content was the highest among ginsenosides in all treatments. The contents total of ginsenosides in all treatments, except EC 8 treatment, was higher than those in the controlled treatment. The PT/PD value was 1.31 of the lowest in the EC 8 treatment and was 2.52 of the highest in the EC6 treatment. Rf contents in high increase was detected at all treated ginseng roots.
The effect of ginsenoside-Rb2, one of a major pharmacological component of Panax ginseng C.A. Meyer, on low density lipoprotein (LDL) receptor expression was investigated and compared with hypocholesterolemic drug lovastatin. In HepG2 cell, exogenous cholesterol decreased LDL receptor mRNA expression, but ginsenoside-Rb2 recovered this reduction of LDL receptor mRNA up to normal expression level. Lovastatin also increased LDL receptor mRNA expression as similar as ginsenoside-Rb2 did. The reduction of sterol regulatory element binding protein (SREBP) transcription by exogenous cholesterol was also similarly recovered by ginsenoside-Rb2 and lovastatin addition. Compound K, a metabolite of ginsenoside-Rb2 and -Rb1 by human intestinal bacteria also increased the SREBP mRNA expression in cholesterol-enriched condition. Ginsenoside-Rb2 seems to up-regulate LDL receptor mRNA expression through the induction of de novo SREBP transcription. Therefore, increased expression of SREBP mRNA by ginsenoside-Rb2 elevated the LDL receptor mRNA expression in HepG2 cells, and these inductions possibly drop the plasma cholesterol level in hypercholesterolemia patients, in vivo, as likely in case of lovastatin.
The binding of bay region diol-epoxides of polycyclic aromatic hydrocarbons (PAHs) to target tissue DNA is thought to be essential for the initiation of cancer by these compounds. In this study we investigated the effect of polyacetylenes such as panaxynol and panaxydol on the formation of benzo(a)pyreno (BP)-metabolite-DNA adduct in the liver of ICR mice. Treatment of mice by i.p. administration of polyacetylenes produced a marked reduction in BP metabolite binding to DNA in vitro. Following i.v. administration of (3H)BP(300, ${\mu}$Ci/21 nmoles/0.1 nt DMSO) to mice, radioactivity was detected in the DNA of the liver in vivo. The result of tentative identification of the 4 peaks between the two standard markers for high pressure liquid chromatography showed that the peaks. I, II, III, and IV were BP-phenol oxide-DNA adduct (or BP-diol-epoxide-dCyt. adduct), (-) BP$.$diolepoxide I:dGuO adduct, (+) BP-diol-epoxide I: dGuo adduct, and BP-diol-epoxide II:dGuO adduct, respectively. The minor adduct, (-) BP-diol epoxide I: dGuo was reduced to 6971 of the amount of the control, while the major adduct, (+) BP-diolepoxide I: dGuO(peak II) which was produced from (-) BP-7, 8-diol was reduced to 78% of that of the control. The amount of the minor adduct, BP-diol-epoxide II:dGuo adduct(peak IV) which formed from (+) BP-7, 8-diol was 58% of the control. These results show that the panaxydol is more related to inhibition of the formation of the minor ad- ducts than of the major adducts, which were generally produced from ($\pm$) BP-7, 8-dihydro-dials.
Chlamydospores were isolated from hyphae of Cylindrocanon destmctans by homogenization and/or ultrasonic treatment. Rate of the isolated chlamydospores by the homogenization with glass tissue grinder were 9.8% of all total chlamydospores formed in the culture of C. destructans. The length of mycelial fragments after the homogenization was about 400㎛ They were, however, formed in clusters of the chlamydospores and the mycelia The rate of the isolated chlamydospores from additional ultrasonic treatment after the homogenization of the mycelia were 74.3%. The length of mycelial fragments with the ultrasonic treatment was about 20 fm and chlamydospores seemed to be isolated from the mycelial mats and dispersed evenly in the culture. The numbers of chlamydospore in a catena were 1 to 8 cells after the homogenization on potato dextrose agar (PDA). Meanwhile the numbers of them after added ultrasonic treatment were 1 to 4 cells. Germination percentages of the isolated chlamydospores from the ultrasonic treatment were 46.8% after incubation of 2 days on PDA at 20。C and 60.7% after incubation of 13 days at 5。C, respectively. Germination rate of chlamydospores to the total chlamydospores produced by the ultrasonic treatment was 55.8%. However, it was increased to 74% when it was measured in the germinated catenae to the total catenae.
Compound K (CK) is a final metabolite of panaxadiol ginsenosides. Although panax ginseng is known to have anti-diabetic activity, the active ingredient is not yet fully identified. Therefore, it would be interesting to know whether and how CK has an anti-diabetic activity. First, insulin secretion-stimulating activity of CK was examined using RIN-m5F cell line and primary cultured islets. CK enhanced the insulin secretion in a concentration dependent manner. This effect, however, was almost completely abolished in the presence of diazoxide, $K^+$ channel opener, indicating that the insulin secretion-stimulating activity of CK is presumably due to blockade of ATP sensitive $K^+$ channel. In addition, effects of CK on gene expressions of hepatic enzymes (phosphoenolpyruvate carboxykinase[PEPCK], glucose-6-phos-phatase[G6Pase]) and on adipocyte differentiation in H4IIE and 3T3-Ll cells, respectively, were examined. CK suppressed the induction of PEPCK and G6Pase mRNA expressions under the dexamethasone/cAMP stimulation condition. CK also reduced the $PPAR-{\gamma}$ mRNA expression and triglyceride accumulation in a dose dependent manner as compared to the control. The present study suggests that CK deserves to examine whether it shows an anti-diabetic activity in animal and human studies.
In this study, we have investigated the effect of panaxatriol (PT) on phosphoinositides (PIS) breakdown and $Ca^{2+}$-elevation in thrombin-induced platelet aggregation. Thrombin (5U/ml), a potent platelet agonist which activates phospholipase $C_{\beta}$ via protease activated receptor (PAR), hydrolyzed PIS in platelet membrane. The phosphatidylinositol 4, 5-bisphosphate $(PIP_2)$ was hydrolyzed after 10 sec of the thrombin-stimulation, and both the phosphatidylinositol 4-monophosphate (PIP) and phosphatidylinositol (PI) were brokendown after 30 sec of the thrombin-stimulation. However, PT inhibited the thrombin-stimulated hydrolysis of $PIP_2$, PIP, and PI. On the other hand, thrombin increased the level of phosphatidic acid (PA) which is phosphorylated from diacylglycerol (DG) generated by PIS-hydrolysis. However, Pr inhibited the thrombin-increased PA level non-significantly. Thrombin increased cytosolic free $Ca^{2+}([Ca^{2+}])_i$) up to 72% as compared with control $(30.8{\pm}0.9 nM)$ in intact platelet. However, PT (100 ${\mu}g/ml$) inhibited the thrombin-elevated $[Ca^{2+}]_i$ to 100%. These results suggest that PT may have a beneficial effect on platelet aggregation-mediated thrombotic disease by inhibiting thrombin-induced platelet aggregation via suppression of the $[Ca^{2+}]_i$ level and PIS breakdown.
Background: Ginsenoside Rg1 is a class of steroid glycoside and triterpene saponin in Panax ginseng. Many studies suggest that Rg1 suppresses adipocyte differentiation in 3T3-L1. However, the detail molecular mechanism of Rg1 on adipogenesis in 3T3-L1 is still not fully understood. Methods: 3T3-L1 preadipocyte was used to evaluate the effect of Rg1 on adipocyte development in the differentiation in a stage-dependent manner in vitro. Oil Red O staining and Nile red staining were conducted to measure intracellular lipid accumulation and superoxide production, respectively. We analyzed the protein expression using Western blot in vitro. The zebrafish model was used to investigate whether Rg1 suppresses the early stage of fat accumulation in vivo. Results: Rg1 decreased lipid accumulation in early-stage differentiation of 3T3-L1 compared with intermediate and later stages of adipocyte differentiation. Rg1 dramatically increased CAAT/enhancer binding protein (C/EBP) homologous protein-10 (CHOP10) and subsequently reduced the $C/EBP{\beta}$ transcriptional activity that prohibited the initiation of adipogenic marker expression as well as triglyceride synthase. Rg1 decreased the expression of extracellular signal-regulated kinase 1/2 and glycogen synthase kinase $3{\beta}$, which are also essential for stimulating the expression of $CEBP{\beta}$. Rg1 also reduced reactive oxygen species production because of the downregulated protein level of nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidase 4 (NOX4). While Rg1 increased the endogenous antioxidant enzymes, it also dramatically decreased the accumulation of lipid and triglyceride in high fat diet-induced obese zebrafish. Conclusion: We demonstrated that Rg1 suppresses early-stage differentiation via the activation of CHOP10 and attenuates fat accumulation in vivo. These results indicate that Rg1 might have the potential to reduce body fat accumulation in the early stage of obesity.
Background: Ginsenoside Rb1, a bioactive component isolated from the Panax ginseng, acts as a remedy to prevent myocardial injury. However, it is obscure whether the cardioprotective functions of Rb1 are related to the regulation of endogenous metabolites, and its potential molecular mechanism still needs further clarification, especially from a comprehensive metabolomics profiling perspective. Methods: The mice model of acute myocardial ischemia (AMI) and oxygen glucose deprivation (OGD)-induced cardiomyocytes injury were applied to explore the protective effect and mechanism of Rb1. Meanwhile, the comprehensive metabolomics profiling was conducted by high-performance liquid chromatography and quadrupole time-of-flight mass spectrometry (HPLC-Q/TOF-MS) and a tandem liquid chromatography and mass spectrometry (LC-MS). Results: Rb1 treatment profoundly reduced the infarct size and attenuated myocardial injury. The metabolic network map of 65 differential endogenous metabolites was constructed and provided a new inspiration for the treatment of AMI by Rb1, which was mainly associated with mitophagy. In vivo and in vitro experiments, Rb1 was found to improve mitochondrial morphology, mitochondrial function and promote mitophagy. Interestingly, the mitophagy inhibitor partly attenuated the cardioprotective effect of Rb1. Additionally, Rb1 markedly facilitated the phosphorylation of AMP-activated protein kinase α (AMPKα), and AMPK inhibition partially weakened the role of Rb1 in promoting mitophagy. Conclusions: Ginsenoside Rb1 protects acute myocardial ischemia injury through promoting mitophagy via AMPKα phosphorylation, which might lay the foundation for the further application of Rb1 in cardiovascular diseases.
Background: Ginsenoside Rb2, a major active component of Panax ginseng, has various physiological activities, including anticancer and anti-inflammatory effects. However, the mechanisms underlying the rejuvenation effect of Rb2 in human skin cells have not been elucidated. Methods: We performed a senescence-associated β-galactosidase staining assay to confirm cellular senescence in human dermal fibroblasts (HDFs). The regulatory effects of Rb2 on autophagy were evaluated by analyzing the expression of autophagy marker proteins, such as microtubule-associated protein 1A/1B-light chain (LC) 3 and p62, using immunoblotting. Autophagosome and autolysosome formation was monitored using transmission electron microscopy. Autophagic flux was analyzed using tandem-labeled GFP-RFP-LC3, and lysosomal function was assessed with Lysotracker. We performed RNA sequencing to identify potential target genes related to HDF rejuvenation mediated by Rb2. To verify the functions of the target genes, we silenced them using shRNAs. Results: Rb2 decreased β-galactosidase activity and altered the expression of cell cycle regulatory proteins in senescent HDFs. Rb2 markedly induced the conversion of LC3-I to LC3-II and LC3 puncta. Moreover, Rb2 increased lysosomal function and red puncta in tandem-labeled GFP-RFP-LC3, which indicate that Rb2 promoted autophagic flux. RNA sequencing data showed that the expression of DNA damage-regulated autophagy modulator 2 (DRAM2) was induced by Rb2. In autophagy signaling, Rb2 activated the AMPK-ULK1 pathway and inactivated mTOR. DRAM2 knockdown inhibited autophagy and Rb2-restored cellular senescence. Conclusion: Rb2 reverses cellular senescence by activating autophagy via the AMPK-mTOR pathway and induction of DRAM2, suggesting that Rb2 might have potential value as an antiaging agent.
This study was carried out to investigate the effect of seasonal changes on some of the morphological and physiological characteristics, including the photosynthetic abilities and dark respiration, of young ginseng plants due to planting location under shading. The results obtained are as follows: 1. Seedlings and 2-year old plants planted in the back rows appeared to have broader leaf area, and their leaf weight greatly increased in September. Chlorophyll content was significantly reduced in September rather than in June and the plants in the back rows had more chlorophyll content than those in the front rows. 2. There was no difference in the light compensation point between the front and back rows in June, while in September the light compensation point of 2-year old ginseng leaves was much lower for plants in the back rows compared with those in the front rows. A difference in the light saturation point was not noticeable between plants in the front and back rows in June and September. But the light saturation point of 2-year old ginseng leaves at $15^{\circ}C$ was high in June, while it was high at $20^{\circ}C$ high in September. 3. Maximum photosynthetic ability was attained at $15^{\circ}C$ in June and at $20^{\circ}C$ in September. During June no significant difference in photosynthetic ability was found between plants in the front and back rows, but in September the amount of photosynthesis was significantly increased at the leaves of seedlings as well as 2-year old plants planted in the back rows. 4. The optimum temperature for maximum photosynthesis in 2-year old plants ranged from $14.0^{\circ}C$ to $14.5^{\circ}C$ in June and from $19.5^{\circ}C$ to $20.5^{\circ}C$ in September. However, the optimum temperature for maximum photosynthesis in the seedlings was from $21.2^{\circ}C$ to $21.6^{\circ}C$ in September, but a significant difference in the optimum temperature for the maximum photosynthesis in seedlings and 2-year old plants was not noticeable between the front and back rows. 5. The respiration rate was rather high in seedlings compared with 2-year old plants. During September the respiration rate in seedlings was much lower in the back rows than in the front rows. The rate of increase in the respiration of 2-year old plants was higher at September than June. The increase in respiration rate due to temperature was more significant in seedlings than 2-year old plants. 6. In September, the level of $Q_{10}$ in 2-year old plants was much lower than that found in seedlings. During June, 2-year old plants showed lower $Q_{10}$ levels at a temperature difference between $15^{\circ}C$ and $25^{\circ}C$; but in September this occurred at a temperature difference between $20^{\circ}C$ and $30^{\circ}C$.
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