Miuraea migitae, a new record of the order Bangiales (Bangiophyceae, Rhodophyta) from Korea

Abstract We found specimens of foliose Bangiales from the subtidal zone of Udo, Jeju Island, Korea. In molecular analyses of rbcL sequences, these Korean specimens were almost identical to Miuraea migitae from Osaka, Japan. In the morphological comparison, Korean specimens were consistent with habitat, color, and vegetative characteristics with the description of M. migitae. This is the first record of M. migitae outside the type locality and Nagasaki in Japan. This study confirms that new or unrecorded species of the order Bangiales may be discovered from subtidal habitats

Methyl 4-(β-D-glucopyranosyloxy)-3-hydroxy-5- methoxybenzoate, isolated from Sanguisorba officinalis, inhibits CpG-DNA-induced inflammation

Purpose: To evaluate the anti-inflammatory effect of methyl-4-(β-D-glucopyranosyloxy)-3-hydroxy-5-methoxybenzoate (comp-1) on immune cells.Methods: Comp-1 was isolated from Sanguisorba officinalis. After treating with comp-1, cell viability and levels of pro-inflammatory cytokines were assessed utilizing MTT assay and ELISA, respectively. Besides, the effects of comp-1 on nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and iNOS were determined using western blotting. Moreover, nitric oxide production was assessed using the Griess reagent.Results: Treatment of dendritic cells (DCs) with CpG DNA upregulated cytokine expression. Comp-1 markedly downregulated the expressions of IL-12 p40, IL-6, and TNF-α, with 50% inhibitory concentrations (IC50) of 1.077 ± 0.04 (p < 0.01), 0.28 ± 0.01 (p < 0.01), and 0.79 ± 0.02 μM (p < 0.01),respectively. Treatment of DCs with CpG DNA upregulated NF-κB and MAPK activation. However, pretreatment of the cells with Comp-1 suppressed CpG DNA-induced NF-κB and MAPK activation. Moreover, comp-1 exhibited a strong anti-inflammatory effect by inhibiting nitric oxide production and iNOS expression.Conclusion: These results reveal that comp-1 has significant anti-inflammatory effect on immune cells. Keywords: Natural compound, Inflammation, Pro-inflammatory cytokine, Toll-like receptor

A designed angiopoietin-2 variant, pentameric COMP-Ang2, strongly activates Tie2 receptor and stimulates angiogenesis

AbstractDespite that angiopoietin-2 (Ang2) produces more versatile and dynamic functions than angiopoietin-1 (Ang1) in angiogenesis and inflammation, the molecular mechanism that underlies this difference is still unknown. To define the role of oligomerization of Ang2 in activation of its receptor, Tie2, we designed and generated different oligomeric forms of Ang2 by replacement of the amino-terminal domains of Ang2 with dimeric, tetrameric, and pentameric short coiled-coil domains derived from GCN4, matrillin-1, and COMP. COMP-Ang2 strongly binds and activates Tie2, whereas GCN4-Ang2 and MAT-Ang2 weakly to moderately bind and activate Tie2. Although native Ang2 strongly binds to Tie2, it does not activate Tie2. Accordingly, COMP-Ang2 strongly promotes endothelial cell survival, migration, and tube formation in a Tie2-dependent manner, and the potency of COMP-Ang2 is almost identical to that of COMP-Ang1. Furthermore, the potency of COMP-Ang2-induced enhanced angiogenesis in the wound healing region is almost identical to the potency of COMP-Ang1-induced enhanced angiogenesis. Overall, there is no obvious difference between COMP-Ang2 and COMP-Ang1 in in vitro and in vivo angiogenesis. Our results provide compelling evidence that proper oligomerization of Ang2 is a critical determinant of its binding and activation of Tie2

Acanthopanax koreanum Fruit Waste Inhibits Lipopolysaccharide-Induced Production of Nitric Oxide and Prostaglandin E2 in RAW 264.7 Macrophages

The Acanthopanax koreanum fruit is a popular fruit in Jeju Island, but the byproducts of the alcoholic beverage prepared using this fruit are major agricultural wastes. The fermentability of this waste causes many economic and environmental problems. Therefore, we investigated the suitability of using A. koreanum fruit waste (AFW) as a source of antiinflammatory agents. AFWs were extracted with 80% EtOH. The ethanolic extract was then successively partitioned with hexane, CH2Cl2, EtOAc, BuOH, and water. The results indicate that the CH2Cl2 fraction (100 μg/mL) of AFW inhibited the LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW 264.7 cells by 79.6% and 39.7%, respectively. These inhibitory effects of the CH2Cl2 fraction of AFWs were accompanied by decreases in the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins and iNOS and COX-2 mRNA in a dose-dependent pattern. The CH2Cl2 fraction of AFWs also prevented degradation of IκB-α in a dose-dependent manner. Ursolic acid was identified as major compound present in AFW, and CH2Cl2 extracts by high performance liquid chromatography (HPLC). Furthermore using pure ursolic acid as standard and by HPLC, AFW and CH2Cl2 extracts was found to contain 1.58 mg/g and 1.75 mg/g, respectively. Moreover, we tested the potential application of AFW extracts as a cosmetic material by performing human skin primary irritation tests. In these tests, AFW extracts did not induce any adverse reactions. Based on these results, we suggest that AFW extracts be considered possible anti-inflammatory candidates for topical application

Safety Evaluation of Yukmijihwang-tang: Assessment of Acute and Subchronic Toxicity in Rats

Yukmijihwang-tang (YMJ; Liu wei di huang tang (China), Rokumigan (Japan)) has been used in the treatment of diseases including renal disorder, cognitive vitality, and diabetes mellitus. However, there is very little information regarding the toxicity of YMJ to give an assurance of safety for clinical treatment. To provide safety information for YMJ, we evaluated its acute and sub-chronic toxicity in rats. The single-dose toxicity of YMJ was examined using Sprague-Dawley rats. Rats were treated with YMJ extract orally at 0, 500, 1000, or 2000 mg/kg body weight. After a single administration, clinical signs were observed every day for two weeks, and body weights were measured five times, including an initial measurement on day 1 (the day of administration). In the sub-chronic oral toxicity study, YMJ was administered to rats at 0, 500, 1000, or 2000 mg/kg/day for 13 weeks. Mortalities, clinical signs, body weight changes, food and water consumption, ophthalmologic findings, urinalysis, hematological and biochemical parameters, gross findings, organ weights, and histological examination were monitored during the study period. We found no mortality and no abnormalities in clinical signs, body weights, and necropsy findings for any of the animals in the acute and sub-chronic studies following oral administration in the rat at up to 2000 mg/kg/day YMJ. YMJ may not have any single-dose toxicity; the LD50 of YMJ was over 2000 mg/kg, and it is safe for rats. The no-observed-adverse-effect-level (NOAEL) was considered to be 2000 mg/kg/day

Proteomic and biochemical analyses reveal the activation of unfolded protein response, ERK-1/2 and ribosomal protein S6 signaling in experimental autoimmune myocarditis rat model

<p>Abstract</p> <p>Background</p> <p>To investigate the molecular and cellular pathogenesis underlying myocarditis, we used an experimental autoimmune myocarditis (EAM)-induced heart failure rat model that represents T cell mediated postinflammatory heart disorders.</p> <p>Results</p> <p>By performing unbiased 2-dimensional electrophoresis of protein extracts from control rat heart tissues and EAM rat heart tissues, followed by nano-HPLC-ESI-QIT-MS, 67 proteins were identified from 71 spots that exhibited significantly altered expression levels. The majority of up-regulated proteins were confidently associated with unfolded protein responses (UPR), while the majority of down-regulated proteins were involved with the generation of precursor metabolites and energy metabolism in mitochondria. Although there was no difference in AKT signaling between EAM rat heart tissues and control rat heart tissues, the amounts and activities of extracellular signal-regulated kinase (ERK)-1/2 and ribosomal protein S6 (rpS6) were significantly increased. By comparing our data with the previously reported myocardial proteome of the Coxsackie viruses of group B (CVB)-mediated myocarditis model, we found that UPR-related proteins were commonly up-regulated in two murine myocarditis models. Even though only two out of 29 down-regulated proteins in EAM rat heart tissues were also dysregulated in CVB-infected rat heart tissues, other proteins known to be involved with the generation of precursor metabolites and energy metabolism in mitochondria were also dysregulated in CVB-mediated myocarditis rat heart tissues, suggesting that impairment of mitochondrial functions may be a common underlying mechanism of the two murine myocarditis models.</p> <p>Conclusions</p> <p>UPR, ERK-1/2 and S6RP signaling were activated in both EAM- and CVB-induced myocarditis murine models. Thus, the conserved components of signaling pathways in two murine models of acute myocarditis could be targets for developing new therapeutic drugs or methods aimed at treating enigmatic myocarditis.</p

Opalski's Syndrome with Cerebellar Infarction

A 64-year-old man presented with sudden onset of right-sided hemiparesis, headache, gait disturbance, and recurrent vomiting. A physical examination revealed right-sided hemiparesis, right Horner syndrome, ataxia of the right limbs, and diminished sensation on the left side of his body. Diffusion-weighted MRI revealed an acute right lateral medullary infarction extending from the rostral medulla to the upper cervical cord, and an acute cerebellar infarction in the territory of the medial branch of the posterior inferior cerebellar artery. Magnetic resonance angiography revealed suspicious severe stenosis or near occlusion of the proximal and distal parts of the right vertebral artery, and hypoplasia of the left vertebral artery. We diagnosed ipsilateral hemiparesis with lateral medullary infarction (Opalski's syndrome) and concomitant cerebellar infarction