This study was designed to investigate the stability for chemical contents and biological activities of Mahwang-tang (MT) depending on the preservation temperature and periods. MT decoction pouches were preserved for 3 months at room temperature (RT, $23{\pm}1^{\circ}C$) and refrigeration ($4^{\circ}C$). To evaluate the stability of MT decoction, pH and sugar content were estimated. High-performance liquid chromatography analysis were performed to quantify the contents of marker compounds in MT. Anti-inflammatory effects of MT were evaluated to suppress the generation of nitric oxide, prostaglandin $E_2$ and cytokines (tumor necrosis $factor-{\alpha}$ and interleukin-6) in the RAW 264.7 cells stimulated with lipopolysaccharide. Total antioxidant capacity of MT was determined by ABTS radical scavenging activity. The pH of storage method and period showed a tendency to decrease gradually with time. There were no changes in sugar content depending on the preservation temperature and periods of MT decoction. Among the major components of MT, cinnamaldehyde was reduced time-dependently for 3 months of storage at RT. The inflammatory effect and antioxidant capacity of MT were reduced time-dependently at both RT and $4^{\circ}C$. Our results suggest that the preservation period of MT decoction is recommended in refrigeration within 3 months or less rather than at RT.
Dangyuja (Citrus grandis Osbeck) is a native plant growing only on Jeju Island in Korea. In this study, antiinflammatory effect of dangyuja leaves on a murine macrophage cell line was investigated. RAW 264.7 murine macrophage cells were stimulated with lipopolysaccharide (LPS, $1{\mu}g/mL$) to induce expression of pro-inflammatory markers [interleukin (IL)-6 and inducible nitric oxide synthase (iNOS)]. The crude extract (80% MeOH Ex.) and solvent fractions (hexane, $CHCl_3$, EtOAc, BuOH, and $H_2O$ Ex.) were obtained from dangyuja leaves. The $CHCl_3$ fraction inhibited the nitric oxide (NO) and IL-6 production in a dose-dependent manner. Also, the $CHCl_3$ fraction inhibited mRNA expression and protein levels of iNOS in a dose-dependent manner. Furthermore, the $CHCl_3$ fraction inhibited LPS-induced nuclear factor (NF)-${\kappa}B$ activation and phosphorylation of mitogen-activated protein kinases (MAPKs: ERK, JNK, and p38). These results suggest that dangyuja leaves may inhibit LPS-induced production of inflammatory markers by blocking NF-${\kappa}B$ and MAPKs signaling in RAW 264.7 cells.
Jung, Kiwon;An, Jun Min;Eom, Dae-Woon;Kang, Ki Sung;Kim, Su-Nam
Journal of Ginseng Research
/
v.41
no.2
/
pp.188-194
/
2017
Background: Fermented black ginseng (FBG) is processed ginseng by the repeated heat treatment and fermentation of raw ginseng. The protective effect and mechanism of FBG on cisplatin-induced nephrotoxicity was investigated to evaluate its therapeutic potential. Methods: The free radical scavenging activity of FBG was measured using 1,1-diphenyl-2-picrylhydrazyl (DPPH). In addition, the protective effect against cisplatin-induced renal damage was tested in rats. FBG was orally administered every day at a dose of 150 mg/kg body weight for 10 d, and a single dose of cisplatin was administered intraperitoneally (7.5 mg/kg body weight) with 0.9% saline on the $4^{th}$ d. Results: The DPPH radical-scavenging activity of FBG ($IC_{50}=384{\mu}g/mL$) was stronger than that of raw ginseng. The improved DPPH radical-scavenging activity was mediated by the generation phenolic compounds. The decreased cell viability by cisplatin was recovered significantly after treatment with FBG in a dose-dependent manner. Then, the protective effect of FBG on cisplatin-induced oxidative renal damage was investigated in rats. The decreased creatinine clearance levels, which are a reliable marker for renal dysfunction in cisplatin-treated rats, were reduced to the normal level after the administration of FBG. Moreover, FBG showed protective effects against cisplatin-induced oxidative renal damage in rats through the inhibition of $NF-{\kappa}B/p65$, COX-2, and caspase-3 activation. Conclusion: These results collectively show that the therapeutic evidence for FBG ameliorates the nephrotoxicity via regulating oxidative stress, inflammation, and apoptosis.
Background: Heat stress orchestrates neurodegenerative disorders and results in the formation of reactive oxygen species that leads to cell death. Although the immunomodulatory effects of ginseng are well studied, the mechanism by which ginseng alleviates heat stress in the brain remains elusive. Methods: Rats were exposed to intermittent heat stress for 6 months, and brain samples were examined to elucidate survival and antiinflammatory effect after Korean Red Ginseng (KRG) treatment. Results: Intermittent long-term heat stress (ILTHS) upregulated the expression of cyclooxygenase 2 and inducible nitric oxide synthase, increasing infiltration of inflammatory cells (hematoxylin and eosin staining) and the level of proinflammatory cytokines [tumor necrosis factor α, interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6], leading to cell death (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) and elevated markers of oxidative stress damage (myeloperoxidase and malondialdehyde), resulting in the downregulation of antiapoptotic markers (Bcl-2 and Bcl-xL) and expression of estrogen receptor beta and brain-derived neurotrophic factor, key factors in regulating neuronal cell survival. In contrast, KRG mitigated ILTHS-induced release of proinflammatory mediators, upregulated the mRNA level of the antiinflammatory cytokine IL-10, and increased myeloperoxidase and malondialdehyde levels. In addition, KRG significantly decreased the expression of the proapoptotic marker (Bax), did not affect caspase-3 expression, but increased the expression of antiapoptotic markers (Bcl-2 and Bcl-xL). Furthermore, KRG significantly activated the expression of both estrogen receptor beta and brain-derived neurotrophic factor. Conclusion: ILTHS induced oxidative stress responses and inflammatory molecules, which can lead to impaired neurogenesis and ultimately neuronal death, whereas, KRG, being the antioxidant, inhibited neuronal damage and increased cell viability.
Metabolic syndrome, including obesity, glucose intolerance and elevated blood pressure, is related to type 2 diabetes and cardiovascular disease. Previous studies have reported the anti-oxidative, anti-inflammatory and anti-diabetic effects of purple corn extract. We investigated the efficacy of purple corn extract (PC) against high-fat diet (HFD)-induced obesity and glucose intolerance, and examined the underlying mechanisms by analyzing expression of proteins and genes involved in glucose regulation and macrophage infiltration. C57BL/6 mice were fed with normal chow diet (ND), or HFD treated with distilled water (DW, control) or PC, for 10 weeks. Although body weights were similar in the HFD-fed groups, we observed a decrease in the liver and epididymal adipose tissue (EAT) weights, and enhanced glucose tolerance test (GTT) results in the PC group, as compared with DW group. Liver showed increased Akt phosphorylation in the PC-treated mice; however, no changes were observed in the EAT, for all groups. In PC-treated mice, decreased macrophage infiltration was seen in the EAT, with a reduced expression of macrophage marker genes. Finally, proinflammatory cytokine gene expressions were decreased by PC in the EAT, and a modest trend for downregulation was observed in the liver. Hence, we conclude that PC may decrease glucose intolerance by increasing the phosphorylation of Akt and reducing the macrophage infiltration into the EAT.
Background: Fractional exhaled nitric oxide (FeNO) is a non-invasive marker for eosinophilic airway inflammation and a good predictor of response to corticosteroids. There is a need for a reliable and accurate measurement method, as FeNO measurements have been widely used in clinical practice. Our study aimed to compare two FeNO analyzers and derive a conversion equation for FeNO measurements in adults. Methods: We included 99 participants who had chief complaints of chronic cough and difficulty in breathing. The participants underwent concurrent FeNO measurement using NIOX VERO (Circassia AB) and NObreath (Bedfont). We compared the values of the two devices and analyzed their correlation and agreement. We then formulated an equation to convert FeNO values measured by NObreath into those obtained by NIOX VERO. Results: The mean age of the participants was 51.2±17.1 years, with a female predominance (58.6%). Approximately 60% of the participants had asthma. The FeNO level measured by NIOX VERO (median, 27; interquartile range [IQR], 15-45) was significantly lower than that measured by NObreath (median, 38; IQR, 22-58; p<0.001). There was a strong positive correlation between the two devices (r=0.779, p<0.001). Additionally, Bland-Altman plots and intraclass correlation coefficient demonstrated a good agreement. Using linear regression, we derived the following conversion equation: natural log (Ln) (NObreath)=0.728×Ln (NIOX VERO)+1.244. Conclusion: The FeNO values of NIOX VERO and NObreath were in good agreement and had positive correlations. Our proposed conversion equation could help assess the accuracy of the two analyzers.
Park, Hee-Jin;Song, Jungsik;Park, Yong-Beom;Lee, Soo-Kon;Lee, Sang-Won
The Korean journal of internal medicine
/
v.33
no.6
/
pp.1234-1240
/
2018
Background/Aims: Red blood cell distribution width (RDW) is a value representing the heterogeneity in the size of red blood cell, and it is usually used in distinguishing types of anaemia. Recently, it was reported that it could reflect the burden of inflammation in diverse diseases and their prognosis. Hence, in this study, we investigated whether RDW may contribute to discriminating adult onset Still's disease (AOSD) from sepsis in serious febrile patients within 24 hours after hospitalization. Methods: We reviewed the medical records and enrolled 21 AOSD patients, 27 sepsis patients and 30 matched healthy controls. We collected at least two laboratory results of variables including RDW within 24 hours after hospitalization, and we calculated their mean values. Results: Sepsis patients showed the significantly increased median white blood cell count, compared to AOSD patients ($14,390.0/mm^3$ vs. $12,390.0/mm^3$, p = 0.010). The median RDW in sepsis patients was higher than that in AOSD patients (15.0% vs. 13.3%, p = 0.001), and furthermore, the median RDW in both patient-groups was significantly higher than that in healthy controls. In contrast, the median ferritin level in sepsis patients was lower than that in AOSD patients (544.0 mg/dL vs. 3,756.6 mg/dL, p = 0.001). In multivariate analysis, RDW ${\geq}14.8%$ (odds ratio, 17.549) and ferritin < 2,251.0 mg/dL (odds ratio, 32.414) independently suggested sepsis more than AOSD in patients initially presenting with fever requiring hospitalization. Conclusions: RDW might be a rapid and helpful marker for a differential diagnosis between AOSD from sepsis at an early phase.
Objective: To examine the regulatory effects of exercise on myokine expression in horse skeletal muscle cells, we compared the expression of several myokine genes (interleukin 6 [IL-6], IL-8, chemokine [C-X-C motif] ligand 2 [CXCL2], and chemokine [C-C motif] ligand 4 [CCL4]) after a single bout of exercise in horses. Furthermore, to establish in vitro systems for the validation of exercise effects, we cultured horse skeletal muscle cells and confirmed the expression of these genes after treatment with hydrogen peroxide. Methods: The mRNA expression of IL-6, IL-8, CXCL2, and CCL4 after exercise in skeletal muscle tissue was confirmed using quantitative-reverse transcriptase polymerase chain reactions (qRT-PCR). We then extracted horse muscle cells from the skeletal muscle tissue of a neonatal Thoroughbred. Myokine expression after hydrogen peroxide treatments was confirmed using qRT-PCR in horse skeletal muscle cells. Results: IL-6, IL-8, CXCL2, and CCL4 expression in Thoroughbred and Jeju horse skeletal muscles significantly increased after exercise. We stably maintained horse skeletal muscle cells in culture and confirmed the expression of the myogenic marker, myoblast determination protein (MyoD). Moreover, myokine expression was validated using hydrogen peroxide ($H_2O_2$)-treated horse skeletal muscle cells. The patterns of myokine expression in muscle cells were found to be similar to those observed in skeletal muscle tissue. Conclusion: We confirmed that several myokines involved in inflammation were induced by exercise in horse skeletal muscle tissue. In addition, we successfully cultured horse skeletal muscle cells and established an in vitro system to validate associated gene expression and function. This study will provide a valuable system for studying the function of exercise-related genes in the future.
Previous studies have suggested that rice bran oil (RBO), an edible oil from the byproducts of rice milling, has anti-inflammatory effects in inflammation inducing macrophages, known as M1 subsets. Yet the effects of RBO on the counterpart M2 subsets, the "healing" macrophages, were poorly investigated to date. In this regard, recent studies on the molecular/cellular anti-inflammatory mechanisms of dietary components have demonstrated that mitochondrial respiration contributes to macrophage functioning. Therefore, the current study examined whether RBO regulates cytokine secretion by modulating mitochondrial metabolism in wound healing M2 subsets. Palm oil (PO), enriched with medium-chain fatty acids, served as a positive control. C57BL/6 mice were fed a diet containing either corn oil (CO), PO or RBO for 4 weeks, followed by purification of bone marrow-derived macrophages (BMDM) from their tibias and femurs. Cells were further polarized to M2-BMDM, and the expression of M2 marker (CD206) on cellular surfaces were not affected by dietary intervention. In addition, the secretion of anti-inflammatory cytokine (IL-10) in the culture supernatant was not affected by dietary lipids. Oxygen consumption rate, the indicator of mitochondrial respiration in M2-BMDM was not regulated by RBO intervention and PO treatment. Taken together, this study imply that RBO did not intervene both the regulation of inflammatory responses and mitochondrial respiration in M2 macrophages.
Objectives : Modified Bo-Yang-Hwan-O-Tang (mBHT) is a polyherbal medicine of twelve herbs traditionally used in the treatment of cerebral and cardiac stroke and vascular dementia. The purpose of this study was to evaluate the neuroprotective effect, pyramidal neuronal cell, inflammation and apoptosis of mBHT against global ischemia in rats. Methods : Global ischemia was produced by two-vessel occlusion(2-VO) in SD male rats. mBHT at dose of 500 mg/kg was orally administrated for 2 weeks or 6 weeks after global ischemia. The histopathological changes of ischemic brain were observed by staining of hematoxylin and eosin (H&E) and Nissl and immunohistochemisty with anti-GFAP (glial fibrillary acidic protein) antibody as a astrocyte marker. The expression of inducible nitric oxide synthase (iNOS) and apoptotic proteins such as Bax, Bcl-2 and caspase-3 was determined by western blot. Results : mBHT treatment significantly inhibited the pyramidal neuronal loss in CA1 of hippocampus of global ischemic rats by 2-VO. mBHT also suppressed the activation of astrocytes in the CA1 at 6 weeks after ischemia. In addition, mBHT significantly increased the expression of anti-apoptotic protein, Bcl-2 on iscemic brain, and significantly attenuated the expression of apoptotic proteins, Bax and caspase-3. Conclusions : These results indicate that mBHT inhibits neuronal cell damage induced in global ischemia by 2-VO, suggesting that mBHT may be a potential candidate for the treatment of vascular dementia.
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