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The crosstalk between bacteria and host autophagy: host defense or bacteria offense
Zheng Lin,Wei Fang,Li Guolin 한국미생물학회 2022 The journal of microbiology Vol.60 No.5
Xenophagy is a specific selective autophagy for the elimination of intracellular bacteria. Current evidence suggests that the processes for host autophagy system to recognize and eliminate invading bacteria are complex, and vary according to different pathogens. Although both ubiquitin-dependent and ubiquitin-independent autophagy exist in host to defense invading bacteria, successful pathogens have evolved diverse strategies to escape from or paralyze host autophagy system. In this review, we discuss the mechanisms of host autophagy system to recognize and eliminate intracellular pathogens and the mechanisms of different pathogens to escape from or paralyze host autophagy system, with a particular focus on the most extensively studied bacteria.
Application of Two Different Tracheal Stents in Small Toy Dogs with Tracheal Collapse
Zhenglin Piao,Young-ung Kim,강진수,이동빈,허수영,김남수 한국임상수의학회 2019 한국임상수의학회지 Vol.36 No.5
Tracheal collapse is a common respiratory disease in dogs. There are many ways to treat tracheal collapse, one of which is the use of an intraluminal stent. In this study, we divided 21 dogs into two groups and implant conventional stents and new nitinol stents. Comparison of two groups was based on following, feature of stent fracture, form of stent migration, clinical sign improvement, complication and prognosis. Approaching was established via Carm under spontaneous breathing and placing a stent at the site of collapse. Using radiographic images, determine stent size accurately. For a comparison of identical condition, all intraluminal stents were placed 10 mm caudal from larynx to 10 mm cranial from carina. In this study, new nitinol stents improve the problems of conventional stents and may be effective in the treatment of tracheal collapse in small dogs.
Korean Red Ginseng attenuates anxiety-like behavior during ethanol withdrawal in rats
Zhao, ZhengLin,Kim, Young Woo,Wu, YiYan,Zhang, Jie,Lee, Ju-Hee,Li, XiaoHua,Cho, Il Je,Park, Sang Mi,Jung, Dae Hwa,Yang, Chae Ha,Kim, Sang Chan,Zhao, RongJie The Korean Society of Ginseng 2014 Journal of Ginseng Research Vol.38 No.4
Background: Korean Red Ginseng (KRG) is known to have antianxiety properties. This study was conducted to investigate the anxiolytic effects of KRG extract (KRGE) during ethanol withdrawal (EW) and the involvement of the mesoamygdaloid dopamine (DA) system in it. Methods: Rats were treated with 3 g/kg/d of ethanol for 28 d, and subjected to 3 d of withdrawal. During EW, KRGE (20 mg/kg/d or 60 mg/kg/d, p.o.) was given to rats once/d for 3 d. Thirty min after the final dose of KRGE, anxiety-like behavior was evaluated in an elevated plus maze (EPM), and plasma corticosterone (CORT) levels were determined by a radioimmunoassay (RIA). In addition, concentrations of DA and 3,4-dihydroxyphenylacetic acid (DOPAC) in the central nucleus of the amygdala (CeA) were also measured by high performance liquid chromatography (HPLC). Results: The EPM test and RIA revealed KRGE inhibited anxiety-like behavior and the over secretion of plasma CORT during EW. Furthermore, the behavioral effect was blocked by a selective DA D2 receptor (D2R) antagonist (eticlopride) but not by a selective DA D1 receptor (D1R) antagonist (SCH23390). HPLC analyses showed KRGE reversed EW-induced decreases of DA and DOPAC in a dose-dependent way. Additionally, Western blotting and real-time polymerase chain reaction (PCR) assays showed that KRGE prevented the EW-induced reductions in tyrosine hydroxylase (TH) protein expression in the CeA and TH mRNA expression in the ventral tegmental area (VTA). Conclusion: These results suggest that KRGE has anxiolytic effects during EW by improving the mesoamygdaloid DA system.
Zhao, ZhengLin,Kim, Sang Chan,Wu, YiYan,Zhang, Jie,Xu, YanJi,Cho, Il Je,Yang, Chae Ha,Lee, Bong Hyo,Zhao, RongJie Elsevier 2014 Neuroscience Letters Vol.567 No.-
The role of neuropeptide Y (NPY) in the central nucleus of amygdala (CeA) in the preventive effects of acupuncture against ethanol withdrawal-induced anxiety was investigated. Rats were treated with 3 g/kg/day of ethanol for 28 days, followed by 3 days of withdrawal. Bilateral acupuncture treatment at HT7 (Shen-Men), PC6 (Nei-Guan) or a non-acupoint was respectively added to the rats during the withdrawal once a day for three days. Enzyme-linked immunosorbent assays and real-time polymerase chain reaction analyses showed there was a significant decrease in NPY protein and mRNA expression in the CeA during ethanol withdrawal, which was reversed by acupuncture at HT7 but neither at PC6 nor at a non-acupoint. Acupuncture at HT7 also greatly inhibited the decrease in cAMP response element-binding protein (CREB) phosphorylation in the CeA. In elevated plus maze tests, a selective NPY Y1 receptor antagonist BIBP 3226 into the CeA before the acupuncture abolished almost completely the anxiolytic effect of acupuncture at HT7. These results suggest that acupuncture at HT7 rescues the depletion of amygdaloid NPY and reverses the decrease in CREB phosphorylation to produce anxiolytic effects during ethanol withdrawal. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
Zhao, ZhengLin,Kim, Sang Chan,Liu, HongFeng,Zhang, Jie,Wang, YuHua,Cho, Il Je,Lee, Bong Hyo,Song, Chang Hyun,Lee, Chul Won,Yang, Chae Ha,Zhao, RongJie,Wu, YiYan Hindawi 2017 Evidence-based Complementary and Alternative Medic Vol.2017 No.-
<P>Acupuncture improves ethanol withdrawal-induced anxiety in rats in an acupoint-dependent manner. Thus, the present study investigated the effects of acupuncture on acute restraint stress- (ARS-) induced anxiety. Male rats were exposed to ARS for 3 h followed by acupuncture at either PC6 (Neiguan), HT7 (Shenmen), or a nonacupoint (tail) once a day for three consecutive days. Five minutes after the third acupuncture treatment, anxiety-like behavior was evaluated in an elevated plus maze (EPM). Additionally, plasma corticosterone (CORT) levels were measured by radioimmunoassay and the concentrations of norepinephrine (NE) and 3-methoxy-4-hydroxy-phenylglycol (MHPG) in the central nucleus of the amygdala (CeA) were determined using high-performance liquid chromatography. Acupuncture at PC6, but not HT7 or a nonacupoint, attenuated anxiety-like behavior, but this attenuation was abolished by a postacupunctural intra-CeA infusion of NE. Acupuncture at PC6 also reduced the oversecretion of plasma CORT and inhibited increases in amygdaloid NE and MHPG induced by ARS. Further, Western blot analyses and real-time polymerase chain reaction assays revealed that acupuncture at PC6 prevented ARS-induced enhancements in the protein and mRNA expressions of tyrosine hydroxylase in the CeA. These results suggest that acupuncture performed specifically at acupoint PC6 reduces ARS-induced anxiety-like behavior by dampening amygdaloid noradrenergic responses.</P>
Zhu Zhenglin,Gao Shengqiang,Chen Cheng,Xu Wei,Xiao Pengcheng,Chen Zhiyu,Du Chengcheng,Chen Bowen,Gao Yan,Wang Chunli,Wang Chunli,Huang Wei 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Despite the high prevalence of osteoarthritis (OA) in older populations, disease-modifying OA drugs (DMOADs) are still lacking. This study was performed to investigate the effects and mechanisms of the small molecular drug salicin (SA) on OA progression. Primary rat chondrocytes were stimulated with TNF-α and treated with or without SA. Inflammatory factors, cartilage matrix degeneration markers, and cell proliferation and apoptosis markers were detected at the mRNA and protein levels. Cell proliferation and apoptosis were evaluated by EdU assays or flow cytometric analysis. RNA sequencing, molecular docking and drug affinity-responsive target stability analyses were used to clarify the mechanisms. The rat OA model was used to evaluate the effect of intra-articular injection of SA on OA progression. We found that SA rescued TNF-α-induced degeneration of the cartilage matrix, inhibition of chondrocyte proliferation, and promotion of chondrocyte apoptosis. Mechanistically, SA directly binds to IRE1α and occupies the IRE1α phosphorylation site, preventing IRE1α phosphorylation and regulating IRE1α-mediated endoplasmic reticulum (ER) stress by IRE1α-IκBα-p65 signaling. Finally, intra-articular injection of SA-loaded lactic-co-glycolic acid (PLGA) ameliorated OA progression by inhibiting IRE1α-mediated ER stress in the OA model. In conclusion, SA alleviates OA by directly binding to the ER stress regulator IRE1α and inhibits IRE1α-mediated ER stress via IRE1α-IκBα-p65 signaling. Topical use of the small molecular drug SA shows potential to modify OA progression.