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Jing‑Fang Xiang,Jian‑Chun Yu,Jian‑You Zhu 한국유전학회 2019 Genes & Genomics Vol.41 No.12
Background MiR-27 has been found to present an overt myocardial expression during cardiogenesis. However, whether miR-27 involves in myocarditis development and the possible molecular mechanism remain unknown. The purpose of this study was to investigate the biological characteristic of miR-27 in LPS-damaged H9c2 cells. Methods H9c2 cells were treated with lipopolysaccharide (LPS, 10 μg/ml) for 12 h to form cell injury. MiR-27 mimic and inhibitor were used to up-regulate or down-regulate miR-27 expression. MTT assay and flow cytometry analysis were conducted to test cell viability and apoptosis. The relative RNA expression level of miR-27 and intercellular adhesion molecule 1 (ICAM1) was determined by qRT-PCR. Luciferase reporter gene assay was utilized to confirm the interaction between miR-27 and ICAM1. Western blot was used to determine the protein expression levels. Results We observed that LPS treatment significantly decreased the level of miR-27 in H9c2 cells. Moreover, LPS exposure suppressed cell viability, promoted cell apoptosis and increased the relative expression of p-NF-κB p65/NF-κB p65 and p-IκBα/IκBα. Up-regulation of miR-27 increased cell proliferation and reduced cell apoptosis, while down-regulation of miR-27 suppressed cell growth and promoted cell apoptosis. ICAM1 was predicted and verified as a target of miR-27, and the expression of ICAM1 is negatively regulated by miR-27. The relative expression of p-NF-κB p65/NF-κB p65 and p-IκBα/ IκBα was dramatically decreased by miR-27 mimic and increased by miR-27 inhibitor. Conclusion Our study illustrated that up-regulation of miR-27 exhibits a protective effect on LPS-damaged H9c2 cells, which may be achieved by regulating ICAM1 and NF-κB signaling.
Combined transcriptomic and proteomic analysis of flubendiamide resistance in Plutella xylostella
Li Jing‐Jing,Jin Ming‐Hui,Wang Nian‐Meng,Yu Qi‐Tong,Shang Ze‐Yu,Xue Chao‐Bin 한국곤충학회 2020 Entomological Research Vol.50 No.10
Diamondback moth (DBM), Plutella xylostella, is an important pest of crucifers worldwide. The extensive use of diamide insecticides has led to DBM resistance in the world, and this presents a serious threat to vegetable production. In the present study, transcriptomic and proteomic analyses were combined to investigate the potential flubendiamide‐resistance mechanism in DBM. The lab‐selected (Rh) and field‐collected (Rb) flubendiamide‐resistant lines of P. xylostella with resistance ratios of 1889.92‐fold and 1250.97‐fold, respectively, were used, as well as a lab‐reared flubendiamide‐susceptible line (S). Compared with the S group, the transcriptomic analysis revealed 151 upregulated and 287 downregulated gene messengers in the Rh group and 432 upregulated and 565 downregulated gene messengers in the Rb group. The most frequently enriched pathways of differentially expressed genes (DEGs) were mainly involved in metabolic pathways. Metabolism related genes, including two P450, two ABC transporters, and three trypsins, were upregulated in the Rh line. Additionally, some P450 genes, trypsin, juvenile hormone (JH), and mucin genes were also upregulated in the Rb line. In proteomic analysis comparisons with the S group, there were 78 upregulated and 90 downregulated proteins in the Rh group and 221 upregulated and 155 downregulated proteins in the Rb group. Further analyses found that three CYP and 11 CYP proteins were over‐expressed in Rh and Rb lines, respectively. Four glutathione S‐transferase (GST) and four UGTs were over‐expressed in Rb line. So, we deduced that the detoxification metabolism may be the main mechanism of flubendiamide resistance in P. xylostella.
폴록사머 및 프로필렌글리콜을 이용한 클로트리마졸 고형 좌제의 물리화학적 특성
현경희,오유경,김정애,공경환,김지현,양준호,배명수,김호동,이종달,장현욱,용철순,최한곤 한국약제학회 2005 Journal of Pharmaceutical Investigation Vol.35 No.2
To develop a clotrimazole-loaded solid suppository with poloxamer and propylene glycol, the melting points of various formulations composed of poloxamer 188 (P 188) and propylene glycol were investigated. The dissolution study of clotrimazole delivered by the suppository composed of P 188 and propylene glycol was performed. The mixtures composed of P 188 and propylene glycol were homogeneous. Propylene glycol affected the melting points of poloxamer mixtures. In particular, the mixture [P 188/propylene glycol (70/30%)] with the melting point of about 32°C was a solid form at room temperature and instantly melted at physiological temperature. Furthermore, propylene glycol affected greatly the dissolution rates of clotrimazole from the suppository. Dissolution mechanism analysis showed the dissolution of clotrimazole was proportional to the time. Our results indicated that the solid suppository with P 188 and propylene glycol would be a candidate of rectal dosage form for clotrimazole.
Anti-VEGF Therapy with Bevacizumab - Limited Cardiovascular Toxicity
Yu, Jing,Cao, Xu-Fen,Zheng, Ye,Zhao, Rong-Cheng,Yan, Li-Qiu,Zhao, Lei,Wang, Jia-Wang Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.24
Purpose: This analysis was conducted to evaluate cardiovascular toxicity of commonly used anti-VEGF therapeutic agent, bevacizumab, in treating patients with cancer. Methods: Clinical studies evaluating the efficacy and safety of bevacizumab-based regimens on response and safety for patients with cancer were identified using a predefined search strategy, allowing cardiovascular toxicity and other side effects of treatment to be estimated. Results: In bevacizumab based regimens, 4 clinical studies including 282 patients with advanced cancer (including gliomas, cervical, breast and ovarian cancer) were considered eligible for inclusion. These bevacizumab-based regimens included docetaxel, irinitecan and carboplatin. Systematic analysis suggested that, of 282 patients treated by bevacizumab based regimens, hypertension and thrombo-embolism occurred in 2.5% (7/282), while only 3 patients reported cardiovascular events (1.1%). No treatment related death occurred in bevacizumab based treatment. Conclusion: This systemic analysis suggests that bevacizumab based regimens are associated with reasonable and accepted cardiovascular toxicity when treating patients with gliomas, cervical, breast and ovarian cancer.
Cortisone and hydrocortisone inhibit human Kv1.3 activity in a non-genomic manner.
Yu, Jing,Park, Mi-Hyeong,Choi, Se-Young,Jo, Su-Hyun Springer-Verlag 2015 Naunyn-Schmiedeberg's archives of pharmacology Vol.388 No.6
<P>Glucocorticoids are hormones released in response to stress that are involved in various physiological processes including immune functions. One immune-modulating mechanism is achieved by the Kv1.3 voltage-dependent potassium channel, which is expressed highly in lymphocytes including effector memory T lymphocytes (TEM). Although glucocorticoids are known to inhibit Kv1.3 function, the detailed inhibitory mechanism is not yet fully understood. Here we studied the rapid non-genomic effects of cortisone and hydrocortisone on the human Kv1.3 channel expressed in Xenopus oocytes. Both cortisone and hydrocortisone reduced the amplitude of the Kv1.3 channel current in a concentration-dependent manner. Both cortisone and hydrocortisone rapidly and irreversibly inhibited Kv1.3 currents, eliminating the possibility of genomic regulation. Inhibition rate was stable relative to the degree of depolarization. Kinetically, cortisone altered the activating gate of Kv1.3 and hydrocortisone interacted with this channel in an open state. These results suggest that cortisone and hydrocortisone inhibit Kv1.3 currents via a non-genomic mechanism, providing a mechanism for the immunosuppressive effects of glucocorticoids.</P>
Assessment of the Cytotoxic and Apoptotic Effects of Chaetominine in a Human Leukemia Cell Line
( Jing Yun Yao ),( Rui Hua Jiao ),( Chang Qing Liu ),( Yu Peng Zhang ),( Wan Guo Yu ),( Yan Hua Lu ),( Ren Xiang Tan ) 한국응용약물학회 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.2
Chaetominine is a quinazoline alkaloid originating from the endophytic fungus Aspergillus fumigatus CY018. In this study, we showed evidence that chaetominine has cytotoxic and apoptotic effects on human leukemia K562 cells and investigated the pathway involved in chaetominine-induced apoptosis in detail. Chaetominine inhibited K562 cell growth, with an IC50 value of 35 nM, but showed little inhibitory effect on the growth of human peripheral blood mononuclear cells. The high apoptosis rates, morphological apoptotic features, and DNA fragmentation caused by chaetominine indicated that the cytotoxicity was partially caused by its pro-apoptotic effect. Under chaetominine treatment, the Bax/Bcl-2 ratio was upregulated (from 0.3 to 8), which was followed by a decrease in mitochondrial membrane potential, release of cytochrome c from mitochondria into the cytosol, and stimulation of Apaf-1. Furthermore, activation of caspase-9 and caspase-3, which are the main executers of the apoptotic process, was observed. These results demonstrated that chaetominine induced cell apoptosis via the mitochondrial pathway. Chaetominine inhibited K562 cell growth and induced apoptotic cell death through the intrinsic pathway, which suggests that chaetominine might be a promising therapeutic for leukemia.
Silencing of PDK1 Gene Expression by RNA Interference Suppresses Growth of Esophageal Cancer
Yu, Jing,Chen, Kui-Sheng,Li, Ya-Nan,Yang, Juan,Zhao, Lu Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8
The current study was conducted to explore the inhibitory effects of a small interfering RNA (siRNA) on 3-phosphoinositide-dependent protein kinase 1 (PDK1) expression in esophageal cancer 9706 (EC9706) cells and the influence on their biological behavior. After transfection of a synthesized PDK1 siRNA, PDK1 mRNA and protein expression and the phosphorylation level of the downstream Akt protein were assessed using RT-PCR and Western blot analysis. Proliferation, apoptosis, cell invasion and in vivo tumor formation capacity were also investigated using MTT, flow cytometry, Transwell invasion trials, and nude mouse tumor transplantion, respectively. PDK1 siRNA effectively suppressed PDK1 mRNA and protein expression, and down-regulated the phosphorylation level of the Akt protein in the EC9706 cells (P < 0.05). It also inhibited cell proliferation and invasion, and promoted apoptosis; such effects were particularly obvious at 48 h and 72 h after transfection (P < 0.05). Growth of transplanted tumors was inhibited in nude mice, with decreased PDK1 expression in tumor tissues. PDK1 may be closely correlated with proliferation, apoptosis and invasion of esophageal cancer cells and thus may serve as an effective target for gene therapy.