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Jin Yuqin,Li Jialing,Ding Liang,Zhao Qing,Song Yuxian,Li Guifeng,Ji Jun,Ni Yanhong,Hu Qingang 대한독성 유전단백체 학회 2022 Molecular & cellular toxicology Vol.18 No.1
Background Oxidative stress is involved in the pathogenesis of various inflammatory diseases, such as periodontitis. When periodontitis occurs, reactive oxygen species (ROS) are overproduced and cannot be balanced by the antioxidant defense system, resulting in tissue damage. Madecassic acid (MA), an abundant triterpenoid in Centella asiatica (L.) Urban, has been used as a wound healing, antiinflammatory, and anticancer agent. Moreover, recent studies have shown that MA has an antioxidative effect, but the underlying mechanism remains unclear. Objective Here, we established an effective oxidative stress model induced by hydrogen peroxide (H 2 O 2 ) in human periodontal ligament fi broblasts (hPDLFs) to investigate the antioxidant and protective effects of MA against cell damage and its underlying mechanism of action. Results Pretreatment with MA inhibited cell apoptosis and promoted cell invasion and migration against oxidative injury induced by H 2 O 2 . In addition, MA was able to maintain mitochondrial membrane potential (ΔΨm) under oxidative stress. Notably, we found that MA restored redox balance by reducing intracellular ROS production. Furthermore, we investigated apoptosis-related proteins and found that the levels of anti-apoptosis markers Bcl-xL and Bcl-2 were remarkably upregulated, whereas that of the pro-apoptotic marker Bax was strikingly downregulated. Conclusions Collectively, these findings suggest that MA inhibits H 2 O 2 -induced oxidative stress and apoptosis of hPDLFs by reducing intracellular ROS production to maintain ΔΨm stability.
Dong Liu,Tao Sun,Yuqin Hu,Yigang Ding,Baomin Fan,Haitao Wang 한국공업화학회 2023 Journal of Industrial and Engineering Chemistry Vol.125 No.-
The controllable adjustment of pore structure is of great significance for the high capacitive performanceof porous carbon materials. In this research, a versatile K2CO3 activation approach is proposed to adjustand control the porosity of sunflower plate-derived hierarchical porous carbon materials (HPC-x) by controllingthe K2CO3/carbons mass ratio. Notably, the variety of pore types, including micropores, mesoporesand macropores, can be detected at different K2CO3/carbons mass ratios (0 4). Impressively,the specific surface area of optimal HPC-2 material is 2526 m2/g. Compare with the other samples(HPC-1, HPC-3 or HPC-4), the HPC-2 possess superior capacitance activity (369.4 F/g at 0.5 A/g). Ontop of that, the energy density of HPC-2 assembled supercapacitors in 1 M Na2SO4 and 6 M KOH solutionscan even reach 32.6 and 7.3 Wh/kg, respectively.
A Genetic Heterogeneity of Renpenning Syndrome Mapped to Chromosome Xq21-Xqter
Cui, Bin,Sun, Yuming,Sun, Yuqin,Shi, Yuefeng,Pei, Gang,Kong, Xiangyin,Hu, Landian 한국유전학회 2004 Genes & Genomics Vol.26 No.1
Renpenning sysndrome is an X-linked mental retardation associated with short stature, moderate microcephaly, unremakdable facies, and no other neurological abnormality. Renpenning first reported this disorder in a Mennonite family, and using this family, Renpenning Syndrome (RENS) has been mapped to Xp11.2-p11.4 Xu Cs found a Chinses family with an X-linked hereditary disease, and the clinical phenotype is similar to RENS. Recently, we performed the linkage analysis, and the result has shown ht egenetic heterogeneity of Renpenning Syndrome: a suggestive novel locus mapped to Xq21-Xqter in this Chinese family.
Shen Xuefang,Chen Xiangyuan,Wang Jing,Liu Jing,Wang Zhiyao,Hua Qing,Wu Qichao,Su Yanguang,He Huanzhong,Hu Yuqin,Meng Zhipeng,Xiong Wanxia,Zhu Minmin 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-
Hyperglycemia-mediated endothelial inflammation participates in the pathogenesis of cardiovascular complications in subjects with diabetes. Previous studies reported that phosphatase and tensin homolog deleted on chromosome ten (PTEN) and SET8 participate in high glucose-mediated endothelial inflammation. In this study, we hypothesize that SET8 regulates PTEN expression, thus contributing to high glucose-mediated vascular endothelial inflammation. Our data indicated that plasma soluble intercellular adhesion molecule-1 (sICAM-1) and endothelial selectin (e-selectin) were increased in patients with diabetes and diabetic rats. PTEN expression was augmented in the peripheral blood mononuclear cells of patients with diabetes and in the aortic tissues of diabetic rats. Our in vitro study indicated that high glucose increased monocyte/endothelial adhesion, endothelial adhesion molecule expression and p65 phosphorylation in human umbilical vein endothelial cells (HUVECs). Moreover, high glucose led to endothelial inflammation via upregulation of PTEN. Furthermore, high glucose inhibited SET8 expression and histone H4 lysine 20 methylation (H4K20me1), a downstream target of SET8. SET8 overexpression reversed the effects of high-glucose treatment. shSET8-mediated endothelial inflammation was counteracted by siPTEN. Furthermore, SET8 was found to interact with FOXO1. siFOXO1 attenuated high glucose-mediated endothelial inflammation. FOXO1 overexpression-mediated endothelial inflammation was counteracted by siPTEN. H4K20me1 and FOXO1 were enriched in the PTEN promoter region. shSET8 increased PTEN promoter activity and augmented the positive effect of FOXO1 overexpression on PTEN promoter activity. Our in vivo study indicated that SET8 was downregulated and FOXO1 was upregulated in the peripheral blood mononuclear cells of patients with diabetes and the aortic tissues of diabetic rats. In conclusion, SET8 interacted with FOXO1 to modulate PTEN expression in vascular endothelial cells, thus contributing to hyperglycemia-mediated endothelial inflammation.