Adult ; Female ; Humans ; Sclerosis ; pathology ; physiopathology ; Spleen ; pathology ; Splenic Neoplasms ; pathology

To analyze components of Citrus reticulata and salt-processed C. reticulata by ultra-performance liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry (UPLC-Q-TOF/MS), and compared the changes in components before and after being processed with salt. Principal component analysis (PCA) and partial least squares discriminant analysis (OPLS-DA) were adopted to analyze the difference in fingerprint between crude and processed C. reticulata, showing increased content of eriocitrin, limonin, nomilin and obacunone increase in salt-processed C. reticulata. Potential chemical markers were identified as limonin, obacunone and nomilin, which could be used for distinguishing index components of crude and processed C. reticulata.
Benzoxepins ; chemistry ; Chromatography, High Pressure Liquid ; methods ; Citrus ; chemistry ; Discriminant Analysis ; Limonins ; chemistry ; Mass Spectrometry ; methods ; Principal Component Analysis ; methods ; Salts ; chemistry

The transcription factor nuclear factor kappa B (NF-B) is activated in hepatocytes in the pathogenesis of hepatic steatosis. However, the action mechanism of NF-B remains to be established in the hepatic steatosis. In this study, the subunit of NF-B was found to promote the hepatic steatosis through regulation of histone deacetylase 1 (HDAC1) in hepatocytes. The activity was supported by the phenotypes of knockout (-KO) mice and knockout (-KO) mice. Hepatic steatosis was reduced in the -KO mice, but not in the -KO mice. The reduction was a result of inhibition of HDAC1 activity in the -KO cells. Knockdown of gene led to suppression of hepatocyte steatosis in HepG2 cells. A decrease in sterol-regulatory element binding protein 1c (SREBP1c) protein was observed in the liver of -KO mice and in cell with knockdown. The decrease was associated with an increase in succinylation of SREBP1c protein. The study suggests that stabilizes HDAC1 to support the SREBP1c activity in hepatic steatosis in the pathophysiological condition. Interruption of this novel pathway in the -KO, but not the -KO mice, may account for the difference in hepatic phenotypes in the two lines of transgenic mice.

OBJECTIVETo investigate whether the insertion/deletion(I/D) polymorphism in the angiotensin converting enzyme(ACE) gene is associated with essential hypertension in Xinjiang Kazakh isolated population.

METHODSThe study covered 201 hypertensives and 151 normotensive controls in Xinjiang Barlikun Kazakh population. The I/D polymorphism of ACE gene was determined by polymerase chain reaction.

RESULTSThe frequencies of D and I in the hypertensive group (0.44 and 0.56, respectively) were not significantly different from the controls(0.39 and 0.61, respectively, P=0.16). The frequencies of ACE genotypes of DD, ID, and II were 0.18, 0.52, 0.30 in hypertensives respectively and 0.17, 0.43, 0.40 in control group respectively. There was no significant difference in genotypes between hypertensive group and normotensive group (P=0.14).

CONCLUSIONThe results suggested that the I/D polymorphism of ACE gene might not be associated with hypertension in the Kazakh population of Xinjiang Barlikun area.

Asian Continental Ancestry Group ; genetics ; Blood Pressure ; genetics ; China ; ethnology ; Female ; Gene Frequency ; Humans ; Hypertension ; genetics ; INDEL Mutation ; Male ; Middle Aged ; Peptidyl-Dipeptidase A ; genetics ; Polymorphism, Genetic ; Population Groups

In a search for effective PPAR-γ agonists, 110 clinical drugs were screened via molecular docking, and 9 drugs, including parecoxib, were selected for subsequent biological evaluation. Molecular docking of parecoxib to the ligand-binding domain of PPAR-γ showed high binding affinity and relevant binding conformation compared with the PPAR-γ ligand/antidiabetic drug rosiglitazone. Per the docking result, parecoxib showed the best PPAR-γ transactivation in Ac2F rat liver cells. Further docking simulation and a luciferase assay suggested parecoxib would be a selective (and partial) PPAR-γ agonist. PPAR-γ activation by parecoxib induced adipocyte differentiation in 3T3-L1 murine preadipocytes. Parecoxib promoted adipogenesis in a dose-dependent manner and enhanced the expression of adipogenesis transcription factors PPAR-γ, C/EBPα, and C/EBPβ. These data indicated that parecoxib might be utilized as a partial PPAR-γ agonist for drug repositioning study.

In a search for effective PPAR-γ agonists, 110 clinical drugs were screened via molecular docking, and 9 drugs, including parecoxib, were selected for subsequent biological evaluation. Molecular docking of parecoxib to the ligand-binding domain of PPAR-γ showed high binding affinity and relevant binding conformation compared with the PPAR-γ ligand/antidiabetic drug rosiglitazone. Per the docking result, parecoxib showed the best PPAR-γ transactivation in Ac2F rat liver cells. Further docking simulation and a luciferase assay suggested parecoxib would be a selective (and partial) PPAR-γ agonist. PPAR-γ activation by parecoxib induced adipocyte differentiation in 3T3-L1 murine preadipocytes. Parecoxib promoted adipogenesis in a dose-dependent manner and enhanced the expression of adipogenesis transcription factors PPAR-γ, C/EBPα, and C/EBPβ. These data indicated that parecoxib might be utilized as a partial PPAR-γ agonist for drug repositioning study.

The mammalian epididymis not only plays a fundamental role in the maturation of spermatozoa, but also provides protection against various stressors. The foremost among these is the threat posed by oxidative stress, which arises from an imbalance in reactive oxygen species and can elicit damage to cellular lipids, proteins, and nucleic acids. In mice, the risk of oxidative damage to spermatozoa is mitigated through the expression and secretion of glutathione peroxidase 5 (GPX5) as a major luminal scavenger in the proximal caput epididymidal segment. Accordingly, the loss of GPX5-mediated protection leads to impaired DNA integrity in the spermatozoa of aged Gpx5