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Jin-Yi Han3*, Xu Zi Guang, Jyung-Sik Kwak, Ki-Wan Oh, Han-Ik Bae 충북대학교 동물의학연구소 2012 Journal of Biomedical and Translational Research Vol.13 No.1
The anti-inflammatory effect of PHBV/Collagen (PHCP) was examined in a mouse model of lipopolysaccharide (LPS)-induced skin inflammation. Vascular permeability on the back skin was measured by the local accumulation of Evan’s blue dye after subcutaneous injection of LPS (30 μg site-1). Dye leakage in the skin showed a significant increase at 2 h after injection of LPS. This LPS-induced dye leakage was also completely inhibited by HO-1 inhibitor, ZnPP, and antioxidants, including methyl gallate, trolox, and mannitol. To study the possible mechanisms underlying the in vivo anti-inflammatory effect of PHCP against LPS-induced inflammation, we also examined the effects of PHCP on malondialdehyde (MDA) and glutathione levels in skin tissues and found that pretreatment with PHCP resulted in inhibited MDA elevation and a remarkable reduction of glutathione level. In addition, similar results were obtained after pretreatment with antioxidants, including trolox and mannitol, and HO-1 inhibitor, ZnPP. Histopathologically, an influx of neutrophils into the skin dermis was detected between 24 h and 72 h after LPS injection (30, 100 μg site-1), compared to control animals after injection of saline. This increase was greater in mice treated with 100 μg of LPS than in those treated with 30 μg of LPS and was significantly suppressed by pretreatment with PHCP, antioxidants, and HO-1 inhibitor. These results collectively suggest that PHCP has an anti-inflammatory effect against LPS-induced inflammation model in vivo and may be a good candidate for the skin tissue engineering biomedical application primarily through manipulation of the redox state.
An Jin,Xuelian Xiang,Yun-Yun Zhu,Heng-Yi Yu,Hui-Fang Pi,Peng Zhang,Han-Li Ruan 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.3
Three new alkaloids, 2a-hydroxy-6-O-n-butyloduline,O-n-butyllycorenine, (-)-N-(chloromethyl)lycoramine(1–3), and a new phenolic compound, ((7S)-7-(4-hydroxyphenyl)-7-hydroxypropyl)-20-methylbenzene-30,60-diol (14), along with ten known alkaloids (4–13), wereisolated from the bulbs of Lycoris aurea collected fromHuaihua County of Hunan Province, China. Their structureswere elucidated by spectroscopic methods includingHRESIMS, UV, IR, and NMR. All the isolated compoundswere tested for their neuroprotective effects against CoCl2and H2O2-induced SH-SY5Y cell death. Compounds 1–7and 10 exhibited significant neuroprotective effects againstCoCl2-induced SH-SY5Y cell injury, while compounds1–5, 7, 10 and 12 showed obvious neuroprotective effectsagainst H2O2-induced SH-SY5Y cell death.
Han, Jin-Yi,Ahn, Sun-Young,Yoo, Jae Hyeon,Nam, Sang-Yoon,Hong, Jin Tae,Oh, Ki-Wan Hindawi Publishing Corporation 2015 BioMed research international Vol.2015 No.-
<P>This experiment was designed to investigate whether 4-O-methylhonokiol (MH), a principal ingredient of <I>Magnolia (M.) officinalis</I> bark, alleviated acute intraperitoneal (i.p.) kainic acid- (KA-) induced brain blood barrier dysfunction (BBBD) <I>via</I> pathological examination and cytological analyses of the brain tissues of mice. KA (10–30 mg/kg) time- and dose-dependently increased the water content of brain tissues and induced edema and encephalopathy. However, pretreatment with MH (5 and 20 mg/kg, i.p.) significantly reduced the water content of the brain compared to that observed in the KA control group. Furthermore, MH significantly and dose-dependently reversed the remarkable variations in evan's blue dye (EBD) staining and malondialdehyde (MDA) levels that were induced by KA (10 mg/kg, i.p.). MH also decreased the elevated seizure scores that were induced by KA (10 mg/kg, i.p.) in mice in a manner similar to scavengers such as DMTU and trolox. Additionally, MH significantly scavenged intracellular ROS and Ca<SUP>2+</SUP> within hippocampal cells. The tight junction seals mediated by claudin (Cld-5) were also found to be modulated by MH. MH efficiently reduced 1,1-diphenyl-2-picrylhydrazyl (DPPH) (IC<SUB>50</SUB>, 52.4 mM) and <SUP>•</SUP>OH with an electron spin resonance (ESR) signal rate constant of 4 × 10<SUP>9</SUP> M<SUP>−1</SUP> · S<SUP>−1</SUP>, which is close to the reactivity of the vitamin E analog trolox. Taken together, these results suggest that MH may enhance radical scavenging in lipid and hydrophobic environments, which may be important for the physiological activity of the barrier.</P>
Han, Seung Jin,Choi, Sung-E,Yi, Sang-A,Lee, Soo-Jin,Kim, Hae Jin,Kim, Dae Jung,Lee, Hyun Chul,Lee, Kwan Woo,Kang, Yup Journal of Endocrinology, Ltd. [etc.] 2012 The Journal of endocrinology Vol.212 No.3
<P>2-Aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) is an activator of glutamate dehydrogenase (GDH), which is a mitochondrial enzyme with an important role in insulin secretion. We investigated the effect of BCH on the high-glucose (HG)-induced reduction in glucose-stimulated insulin secretion (GSIS), the HG/palmitate (PA)-induced reduction in insulin gene expression, and HG/PA-induced β-cell death. We also studied whether long-term treatment with BCH lowers blood glucose and improves β-cell integrity in db/db mice. We evaluated GSIS, insulin gene expression, and DNA fragmentation in INS-1 cells exposed to HG or HG/PA in the presence or absence of BCH. An in vivo study was performed in which 7-week-old diabetic db/db mice were treated with BCH (0.7? g/kg, n = 10) and placebo (n = 10) every other day for 6 weeks. After treatment, an intraperitoneal glucose tolerance test and immunohistological examinations were performed. Treatment with BCH blocked HG-induced GSIS inhibition and the HG/PA-induced reduction in insulin gene expression in INS-1 cells. In addition, BCH significantly reduced HG/PA-induced INS-1 cell death and phospho-JNK level. BCH treatment improved glucose tolerance and insulin secretion in db/db mice. BCH treatment also increased the ratio of insulin-positive β-cells to total islet area (P < 0.05) and reduced the percentage of β-cells expressing cleaved caspase 3 (P < 0.05). In conclusion, the GDH activator BCH improved glycemic control in db/db mice. This anti-diabetic effect may be associated with improved insulin secretion, preserved islet architecture, and reduced β-cell apoptosis.</P>
Efficient Generation of Dopaminergic Neurons from Mouse Ventral Midbrain Astrocytes
Han Jin Yi,Lee Eun-Hye,Kim Sang-Mi,Park Chang-Hwan 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.3
Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by tremors, bradykinesia, and rigidity. PD is caused by loss of dopaminergic (DA) neurons in the midbrain substantia nigra (SN) and therefore, replenishment of DA neurons via stem cell-based therapy is a potential treatment option. Astrocytes are the most abundant non-neuronal cells in the central nervous system and are promising candidates for reprogramming into neuronal cells because they share a common origin with neurons. The ability of neural progenitor cells (NPCs) to proliferate and differentiate may overcome the limitations of the reduced viability and function of transplanted cells after cell replacement therapy. Achaete-scute complex homolog-like 1 (Ascl1) is a wellknown neuronal-specific factor that induces various cell types such as human and mouse astrocytes and fibroblasts to differentiate into neurons. Nurr1 is involved in the differentiation and maintenance of DA neurons, and decreased Nurr1 expression is known to be a major risk factor for PD. Previous studies have shown that direct conversion of astrocytes into DA neurons and NPCs can be induced by overexpression of Ascl1 and Nurr1 and additional transcription factors genes such as superoxide dismutase 1 and SRY-box 2. Here, we demonstrate that astrocytes isolated from the ventral midbrain, the origin of SN DA neurons, can be effectively converted into DA neurons and NPCs with enhanced viability. In addition, when these NPCs are inducted to differentiate, they exhibit key characteristics of DA neurons. Thus, direct conversion of midbrain astrocytes is a possible cell therapy strategy to treat neurodegenerative diseases.