http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Phenolic constituents from Parakmeria yunnanensis and their anti-HIV-1 activity
Shan-Zhai Shang,Huan Chen,Cheng-Qin Liang,Zhong-Hua Gao,Xue Du,Rui-Rui Wang,Yi-Ming Shi,Yong-Tang Zheng,Wei-Lie Xiao,Han Dong Sun 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.10
Three new phenolic compounds, yunnanensinsA–C (1–3), together with fourteen known ones (4–17),were isolated from the leaves and stems of Parakmeriayunnanensis. The structures of new compounds wereestablished on the basis of extensive spectroscopic analyses. Several compounds showed weak anti-HIV-1 activity.
Xiang Zhai,Xin-yang Li,Yu-jing Wang,Ke-ru Qin,Jin-rui Hu,Mei-ning Li,Hai-long Wang,Rui Guo 대한내분비학회 2022 Endocrinology and metabolism Vol.37 No.3
Background: It is well-established that serum testosterone in men decreases with age, yet the underlying mechanism of this changeremains elusive. Methods: The expression patterns of Fancd2 opposite-strand (Fancd2os) in BALB/c male mice and testicular tissue derived celllines (GC-1, GC-2, TM3, and TM4) were assessed using real-time polymerase chain reaction (RT-PCR), Western blot and immunofluorescence. The Fancd2os-overexpressing or knockdown TM3 cells were constructed by infecting them with lentivirus particlesand were used to evaluated the function of Fancd2os. The testosterone production was measured using enzyme linked immunosorbent assay (ELISA) and the steroidogenic enzymes such as steroidogenic acute regulatory protein (StAR), P450 cholesterol sidechain cleavage (P450scc), and 3β-hydroxysteroid dehydrogenase (3β-HSD) were analysed using RT-PCR. The apoptosis of TM3cells induced by ultraviolet light or testicular tissues was detected using flow cytometry, Western blot or dUTP-biotin nick end labeling (TUNEL) assays. Pearson correlation analysis was used to assess the correlation between the Fancd2os expression and TUNELpositive staining in mouse testicular Leydig cells. Results: The Fancd2os protein was predominantly expressed in mouse testicular Leydig cells and its expression increased with age. Fancd2os overexpression inhibited testosterone levels in TM3 Leydig cells, whereas knockdown of Fancd2os elevated testosteroneproduction. Fancd2os overexpression downregulated the levels of StAR, P450scc and 3β-HSD, while Fancd2os knockdown reversed this effect. Fancd2os overexpression promoted ultraviolet light-induced apoptosis of TM3 cells. In contrast, Fancd2os knockdown restrained apoptosis in TM3 cells. In vivo assays revealed that higher Fancd2os levels and mouse age were associated with increased apoptosis in Leydig cells and decreased serum testosterone levels. Pearson correlation analysis exhibited a strong positivecorrelation between the expression of Fancd2os and TUNEL-positive staining in mouse testicular Leydig cells. Conclusion: Our findings suggest that Fancd2os regulates testosterone synthesis via both steroidogenic enzymes and the apoptoticpathway.
Rui Li,Zhen Zhai,Xiaomei Zhang,Tao Liu,Mingxing Jin,Haifeng Xu,Bing Yan 대한화학회 2014 Bulletin of the Korean Chemical Society Vol.35 No.5
The complete active space self-consist field method followed by the internally contracted multireference configuration interaction method has been used to compute the potential energy curves of X2Πg, a4Πu, A2Πu, b4Σ− g, and B2Σ− g states of S2 + cation with large correlation-consistent basis sets. Utilizing the potential energy curves computed with different basis sets, the spectroscopic parameters of these states were evaluated. Finally, the transition dipole moment and the Franck-Condon factors of the transition from A2Πu to X2Πg were evaluated. The radiative lifetime of A2Πu is calculated to be 887 ns, which is in good agreement with experimental value of 805 ± 10 ns.
Rui Ma,Chao Ma,Ruixue Zhai,Jun Zhao 한국정밀공학회 2022 International Journal of Precision Engineering and Vol.23 No.5
The springback control method is usually based on surface compensation to make the shape of the springback consistent with the target. At present, it is mainly realized by theoretical calculation or numerical simulation, but the difference between material model and theoretical model leads to unstable compensation accuracy. In this paper, a compensation mechanism which based on the iterative principle of implicit equation is proposed from the point of view of mathematical analysis. The final shape of the part converges to the target shape by means of finite compensation with the iterative method. In this paper, the iterative compensation mechanism is applied to the free bending and stretch-bending processes under plane stress state, and the uniform curvature and variable curvature are compensated iteratively. The next iteration compensation profile is predicted according to the convergence of the iterative principle. Experimental results show that the iterative compensation method can predict the next compensation value, and the error is less than the target value after 2–3 iterations. The error convergence of the method studied in this project is directional and the convergence speed is fast. The compensation value can be quantitatively predicted, which has theoretical significance and application value for engineering design, mold repair and numerical simulation.
Targeting cathepsin L in the regulation of apoptosis in peripheral T-cell lymphoma
Zhang Rui,Ruan Yanjie,Zhao Yiming,Jin Fengbo,Yang Mingzhen,Zhai Zhimin 대한독성 유전단백체 학회 2024 Molecular & cellular toxicology Vol.20 No.3
Backgrounds Peripheral T-cell lymphoma (PTCL) is a heterogeneous lymphoproliferative neoplasms derived from post-thymic T lymphocytes and mature NK cells. Although the incidence is rare, PTCL is frequently recurrence with pore prognosis. Cathepsin L is a member of cysteine proteases strongly related to the carcinogenesis and progression of malignant tumors. Objectives To test the expression of cathepsin L in PTCL and to clarify the possible role of cathepsin L in the pathogenesis of PTCL. Results The public datasheets showed a significant increase of cathepsin L in PTCL than normal T-cells. This result was confirmed by the collected tumor samples, in which the pathological changes and the immunohistochemical test were consistent with PTCL diagnosis. Two PTCL cell lines, Jurkat and Hut78, with a stable knockdown of cathepsin L were successfully established. The RNAseq analysis reported a total of eight co-differentially expressed genes between cathepsin Llow Jurkat vs vector Jurkat and cathepsin Llow Hut78 vs vector Hut78 two datasheets. The apoptosis array reported abnormal expression of several pro-apoptosis proteins including Fas, Bax, sTNF-R1, IGFBP-6, etc. According to the gene function enrichment analysis, p53 signaling pathway was involved in loss of cathepsin L in PTCL cells in vitro. In addition, the levels of above differentially expressed genes/proteins were finally checked, and our data confirmed an alteration of p53, apoptosis regulation-related factors (PAK4, SESN2) and apoptosis-related factors (Fas, Bax, sTNF-R1, and IGFBP-6). Conclusion Taken together, we demonstrated a role of cathepsin L in apoptosis by regulation of p53 signaling pathway. Our finding might provide a new possible candidate drug target for clinical treatment of PTCL in future. Backgrounds Peripheral T-cell lymphoma (PTCL) is a heterogeneous lymphoproliferative neoplasms derived from post-thymic T lymphocytes and mature NK cells. Although the incidence is rare, PTCL is frequently recurrence with pore prognosis. Cathepsin L is a member of cysteine proteases strongly related to the carcinogenesis and progression of malignant tumors. Objectives To test the expression of cathepsin L in PTCL and to clarify the possible role of cathepsin L in the pathogenesis of PTCL. Results The public datasheets showed a significant increase of cathepsin L in PTCL than normal T-cells. This result was confirmed by the collected tumor samples, in which the pathological changes and the immunohistochemical test were consistent with PTCL diagnosis. Two PTCL cell lines, Jurkat and Hut78, with a stable knockdown of cathepsin L were successfully established. The RNAseq analysis reported a total of eight co-differentially expressed genes between cathepsin Llow Jurkat vs vector Jurkat and cathepsin Llow Hut78 vs vector Hut78 two datasheets. The apoptosis array reported abnormal expression of several pro-apoptosis proteins including Fas, Bax, sTNF-R1, IGFBP-6, etc. According to the gene function enrichment analysis, p53 signaling pathway was involved in loss of cathepsin L in PTCL cells in vitro. In addition, the levels of above differentially expressed genes/proteins were finally checked, and our data confirmed an alteration of p53, apoptosis regulation-related factors (PAK4, SESN2) and apoptosis-related factors (Fas, Bax, sTNF-R1, and IGFBP-6). Conclusion Taken together, we demonstrated a role of cathepsin L in apoptosis by regulation of p53 signaling pathway. Our finding might provide a new possible candidate drug target for clinical treatment of PTCL in future.
Li, Rui,Zhai, Zhen,Zhang, Xiaomei,Liu, Tao,Jin, Mingxing,Xu, Haifeng,Yan, Bing Korean Chemical Society 2014 Bulletin of the Korean Chemical Society Vol.35 No.5
The complete active space self-consist field method followed by the internally contracted multireference configuration interaction method has been used to compute the potential energy curves of $X^2\prod_g$, $a^4\prod_u$, $A^2\prod_u$, $b^4\sum_{g}^{-}$, and $B^2\sum_{g}^{-}$ states of $S{_2}^+$ cation with large correlation-consistent basis sets. Utilizing the potential energy curves computed with different basis sets, the spectroscopic parameters of these states were evaluated. Finally, the transition dipole moment and the Franck-Condon factors of the transition from $A^2\prod_u$ to $X^2\prod_g$ were evaluated. The radiative lifetime of $A^2\prod_u$ is calculated to be 887 ns, which is in good agreement with experimental value of $805{\pm}10$ ns.
Ginsenosides repair UVB-induced skin barrier damage in BALB/c hairless mice and HaCaT keratinocytes
Zhenzhuo Li,Rui Jiang,Manying Wang,Lu Zhai,Jianzeng Liu,Xiaohao Xu,Liwei Sun,Daqing Zhao 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.1
Background: Ginsenosides (GS) have potential value as cosmetic additives for prevention of skin photoaging. However, their protective mechanisms against skin barrier damage and their active monomeric constituents are unknown. Methods: GS monomer types and their relative proportions were identified. A UVB-irradiated BALB/c hairless mouse model was used to assess protective effects of GS components on skin epidermal thickness and transepidermal water loss (TEWL). Skin barrier function, reflected by filaggrin (FLG), involucrin (IVL), claudin-1 (Cldn-1), and aquaporin 3 (AQP3) levels and MAPK phosphorylation patterns, were analyzed in UVB-irradiated hairless mice or HaCaT cells. Results: Total GS monomeric content detected by UPLC was 85.45% and was largely attributed to 17 main monomers that included Re (16.73%), Rd (13.36%), and Rg1 (13.38%). In hairless mice, GS ameliorated UVB-induced epidermal barrier dysfunction manifesting as increased epidermal thickness, increased TEWL, and decreased stratum corneum water content without weight change. Furthermore, GS treatment of UVB-irradiated mice restored protein expression levels and epidermal tissue distributions of FLG, IVL, Cldn-1, and AQP3, with consistent mRNA and protein expression results obtained in UVB-irradiated HaCaT cells (except for unchanging Cldn-1 expression). Mechanistically, GS inhibited JNK, p38, and ERK phosphorylation in UVB-irradiated HaCaT cells, with a mixture of Rg2, Rg3, Rk3, F2, Rd, and Rb3 providing the same protective MAPK pathway inhibition-associated upregulation of IVL and AQP3 expression as provided by intact GS treatment. Conclusion: GS protection against UVB-irradiated skin barrier damage depends on activities of six ginsenoside monomeric constituents that inhibit the MAPK signaling pathway.