Journal: Frontiers in pharmacology

Article Title: Volatile Oil from Amomi Fructus Attenuates 5-Fluorouracil-Induced Intestinal Mucositis.

doi: 10.3389/fphar.2017.00786

Figure Lengend Snippet: FIGURE 5 | Reduced IL-6, ROS, TNF-α, NF-κB, and MPO after VOA and BA treatment in blood and small intestinal tissue (n = 6). Increased (A) IL-6 and (B) ROS in blood after 5-FU. VOA and BA reduced inflammation. Increased (C) ROS, (D) TNF-α, (E) MPO, and (F) NF-κB in small intestinal tissue after 5-FU. VOA and BA reduced pro-inflammatory cytokines. Values are means, with their standard deviation represented by vertical bars. Values are means ± SD. ∗Significant difference compared to the controls. # Significant difference compared to the model and controls. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, #p < 0.05, ##p < 0.01, and ###p < 0.001.

Article Snippet: ROS, tumor necrosis factor-α (TNF-α), nuclear factor of kappa b (NF-κB), and myeloperoxidase MPO in the intestinal homogenate were measured with ELISA kits purchased from Cusabio Biotech Co., Ltd. (China).

Techniques: Standard Deviation

Journal: BMC Molecular and Cell Biology

Article Title: Compression and tension variably alter Osteoprotegerin expression via miR-3198 in periodontal ligament cells

doi: 10.1186/s12860-019-0187-2

Figure Lengend Snippet: miR-3198 gain-of-function and loss-of-function experiments. Results of real-time RT-PCR analysis for miR-3198 ( a , b ), OPG and RANKL ( c , d ) expression in HPL cells after transfection of miR-3198 inhibitor ( a , c ) and miR-3198 mimic ( b , d ). n = 3. Biological triplicated. Fold change from the control is shown. Open bar indicates the fold change of OPG expression, and close bar indicates that of RANKL expression ( c , d ). The concentrations of OPG as measured by ELISA after transfection of miR-3198 inhibitor ( e ) and miR-3198 mimic ( f ) are shown ( n = 3). Results of real-time PCR analysis for miR-1207 ( g , h ), OPG and RANKL ( i , j ) expression in HPL cells under the transfection of miR-1207 inhibitor ( g , i ) and miR-1207 mimic ( h , j ). n = 3. Biological triplicated. Fold changes from the control are shown. * indicates P < 0.05 versus control, and NS indicating there was no significant difference between samples

Article Snippet: The concentration of OPG in the culture supernatant was measured using an OPG ELISA kit (Boster Biological Technology, Pleasanton, CA), according to the manufacturer’s instructions.

Techniques: Quantitative RT-PCR, Expressing, Transfection, Control, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction

Journal: BMC Molecular and Cell Biology

Article Title: Compression and tension variably alter Osteoprotegerin expression via miR-3198 in periodontal ligament cells

doi: 10.1186/s12860-019-0187-2

Figure Lengend Snippet: miR-3198 regulates the mechanical stress-mediated change of OPG expression. Results of real-time RT-PCR analysis for OPG and RANKL expression in HPL cells in the compression ( a ) and tension ( b ) experiments. n = 3. Biological triplicated. Fold change from the control are shown. Cont, control; Inh, transfection of miR-3198 inhibitor; Mimic, transfection of miR-3198 mimic; press, compression; tens, tension; TF, transfection. Also shown are the OPG concentrations measured by ELISA in the compression ( c ) and tension ( d ) experiments ( n = 3). * indicates P < 0.05 versus control. † indicates P < 0.05 between samples. NS indicates there was no significant difference between samples. e and f Representative image of the western blotting for OPG was shown. g and h Relative band intensity of the western blotting for OPG. *: P < 0.05 versus control. †: P < 0.05 between the groups. NS, no significant difference between the samples

Article Snippet: The concentration of OPG in the culture supernatant was measured using an OPG ELISA kit (Boster Biological Technology, Pleasanton, CA), according to the manufacturer’s instructions.

Techniques: Expressing, Quantitative RT-PCR, Control, Transfection, Enzyme-linked Immunosorbent Assay, Western Blot

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Article Title: Reduced Plasma Kallistatin Is Associated With the Severity of Coronary Artery Disease, and Kallistatin Treatment Attenuates Atherosclerotic Plaque Formation in Mice

doi: 10.1161/JAHA.118.009562

Figure Lengend Snippet: Kallistatin inhibited low‐shear stress–induced carotid artery plaque formation. A , Representative magnetic resonance images in cross‐sectional views through the carotid arteries. The red arrow indicates the cross section of the left carotid artery, and the blue arrow indicates the cross section of the right carotid artery. B , Quantitative analysis of left carotid artery diameter in the Ad. HKS and Ad.Null groups. L‐ NAME and NAM blocked the effects of kallistatin (n=10, * P <0.05 vs the Ad.Null‐, L‐ NAME ‐, or NAM ‐treated groups). C , Quantitative analysis of left carotid artery plaque volume in the Ad. HKS and Ad.Null groups. L‐ NAME and NAM blocked the effect of kallistatin; n=10 (* P <0.05 vs the Ad.Null‐, L‐ NAME ‐ or NAM ‐treated groups). D , Plasma MDA levels in apoE −/− mice. E , Plasma TNF ‐α levels in apoE −/− mice. F , Distribution of mouse kallistatin expression in atherosclerotic lesions and normal vascular tissue. Data are presented as the mean± SEM ; n=10, * P <0.05 vs the Ad.Null‐, L‐ NAME ‐, or NAM ‐treated groups. Ad.HKS indicates adenovirus containing kallistatin cDNA; Ad.Null, adenovirus containing null cDNA; L‐NAME, N ω ‐nitro‐L‐arginine methyl ester; MDA, malondialdehyde; NAM, nicotinamide; SEM, standard error of the mean; TNF‐α, tumor necrosis factor‐α.

Article Snippet: Plasma samples were used for the analysis of TNF‐α using a Mouse TNF‐α ELISA (Proteintech, Rosemount, IL) according to the manufacturer's protocol.

Techniques: Shear, Clinical Proteomics, Expressing

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Article Title: Reduced Plasma Kallistatin Is Associated With the Severity of Coronary Artery Disease, and Kallistatin Treatment Attenuates Atherosclerotic Plaque Formation in Mice

doi: 10.1161/JAHA.118.009562

Figure Lengend Snippet: Kallistatin led to morphological changes in the atherosclerotic plaques of apoE −/− mice. A , Representative images of HE staining. Original magnification is ×10 (n=5 in each group). B , Oil red O staining of carotid specimens of mice in the Ad.Null group, the Ad. HKS group, and L‐ NAME ‐ or NAM ‐treated groups (n=5 in each group). C , Representative images of superoxide formation labeled by the red fluorescence dye dihydroethidium in the carotid artery of Ad.Null mice, Ad. HKS mice, Ad. HKS +L‐ NAME mice, and Ad. HKS + NAM mice (n=5 in each group). D , Representative images of CD 68 immunostaining in lesion areas of the left carotid artery (n=5 in each group). E , Immunohistochemical assessments of the protein level of TNF ‐α in carotid plaque (n=5 in each group). F, Quantitative analyses of CD 68‐positive cells in the 4 groups (n=5 in each group, * P <0.05 vs the Ad.Null‐, L‐ NAME ‐, or NAM ‐treated groups). G , Fluorescence intensity was measured by a fluorescence microscope and quantified with Image software (n=5 in each group, * P <0.05 vs the Ad.Null‐, L‐ NAME ‐, or NAM ‐treated groups). H , Colocalization of PE red fluorescence ( SIRT 1) and FITC green fluorescence ( CD 31) within plaques (×40 magnification) in the carotid arteries of the Ad.Null, Ad. HKS , Ad. HKS +L‐ NAME , and Ad. HKS + NAM groups with labeled cell nuclei (blue) (n=5 in each group). Regions shown at a higher magnification (far right) are indicated by yellow boxes. Endothelial cell‐specific SIRT 1 fluorescence was measured on the luminal side of the internal elastic lamina only and expressed in mean pixel intensity per area (n=5 in each group, # P <0.05 vs the Ad.Null‐ and NAM ‐treated groups). I , Colocalization of PE red fluorescence ( eNOS ) and FITC green fluorescence ( CD 31) within carotid artery plaques (×40 magnification) of the 4 groups with labeled cell nuclei (blue). Regions shown at a higher magnification (far right) are indicated by yellow boxes. Endothelial cell‐specific eNOS fluorescence was measured on the luminal side of the internal elastic lamina only and expressed in mean pixel intensity per area (* P <0.05 vs the Ad.Null‐, L‐ NAME ‐, or NAM ‐treated groups). We observed that red fluorescence ( SIRT 1, eNOS ) and green fluorescence ( CD 31) signals were colocalized in the Ad. HKS group. Scale bar=50 μm. Ad.HKS indicates adenovirus containing kallistatin cDNA; Ad.Null, adenovirus containing null cDNA; DAPI, 4′,6‐diamidino‐2‐phenylindole; DHE, dihydroethidium; eNOS, endothelial nitric oxide synthase; FITC, fluoroisothiocyanate; HE, hematoxylin and eosin; L‐NAME, N ω ‐nitro‐L‐arginine methyl ester; NAM, nicotinamide; PE, phycoerythrin; SIRT1, sirtuin 1; TNF‐α, tumor necrosis factor‐α.

Article Snippet: Plasma samples were used for the analysis of TNF‐α using a Mouse TNF‐α ELISA (Proteintech, Rosemount, IL) according to the manufacturer's protocol.

Techniques: Staining, Labeling, Fluorescence, Immunostaining, Immunohistochemical staining, Microscopy, Software

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Article Title: Reduced Plasma Kallistatin Is Associated With the Severity of Coronary Artery Disease, and Kallistatin Treatment Attenuates Atherosclerotic Plaque Formation in Mice

doi: 10.1161/JAHA.118.009562

Figure Lengend Snippet: Effect of kallistatin protein ( KS ) on TNF ‐α–induced HUVEC s. NADPH oxidase activity ( A ), intracellular ROS accumulation ( B ), relative SIRT 1 mRNA expression levels ( C ), relative eNOS mRNA expression levels ( D ), and SIRT 1 and eNOS protein expression ( E ). Data are presented as the mean± SEM (n=5, * P <0.05 vs the TNF ‐α, TNF ‐α+ KS + NAM , and TNF ‐α+ KS + L‐ NAME groups. # P <0.05 vs the TNF ‐α and TNF ‐α+ KS + NAM groups). eNOS indicates endothelial nitric oxide synthase; HUVEC, human umbilical vein endothelial cells; KS, kallistatin; L‐NAME, N ω ‐nitro‐L‐arginine methyl ester; NAM, nicotinamide; ROS, reactive oxygen species; SIRT1, sirtuin 1; TNF‐α, tumor necrosis factor‐α.

Article Snippet: Plasma samples were used for the analysis of TNF‐α using a Mouse TNF‐α ELISA (Proteintech, Rosemount, IL) according to the manufacturer's protocol.

Techniques: Activity Assay, Expressing