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Image Search Results
Journal: iScience
Article Title: The mechanisms and therapeutic potential of clopidogrel in mitigating diabetic cardiomyopathy in db/db mice
doi: 10.1016/j.isci.2024.109134
Figure Lengend Snippet:
Article Snippet:
Techniques: Recombinant, Bicinchoninic Acid Protein Assay, Enzyme-linked Immunosorbent Assay, Activity Assay, Multiple Displacement Amplification, GSSG Assay, Isolation, Reverse Transcription, CCK-8 Assay, ROS Assay, Software
Journal: Journal of Cellular and Molecular Medicine
Article Title: Nesfatin‐1 inhibits myocardial ischaemia/reperfusion injury through activating Akt/ERK pathway‐dependent attenuation of endoplasmic reticulum stress
doi: 10.1111/jcmm.16481
Figure Lengend Snippet: Nesfatin‐1 restoration ameliorates MI/R injury. (A‐E) Mice were intramyocardially administrated with 5 or 10 ng/g bodyweight nesfatin‐1 at 30 min after ischaemia. Each group contains 7 mice. (A) Nesfatin‐1 peptide amount in heart homogenates was measured by ELISA assay. (B) Infarct area in the heart slices was evaluated by TTC staining. (C) The cardiac troponin T level in the serum was assessed using ELISA assay. (D) Myocardial apoptosis was detected by TUNEL staining, and the percentage of apoptotic myocardial cells is depicted on the right. (E) The caspase‐3 activity in heart homogenates was determined by caspase activity assay. Data are mean ± SD (n = 7). Student's t test. *, P < .05; **, P < .01. NS, not significant
Article Snippet: The activity of caspase‐3 was detected by Caspase‐3 Activity Assay Kit (#5723, Cell Signaling Technology), and the LDH activity was assessed by the
Techniques: Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Activity Assay, Caspase Activity Assay
Journal: Journal of Cellular and Molecular Medicine
Article Title: Nesfatin‐1 inhibits myocardial ischaemia/reperfusion injury through activating Akt/ERK pathway‐dependent attenuation of endoplasmic reticulum stress
doi: 10.1111/jcmm.16481
Figure Lengend Snippet: Akt/ERK inhibition significantly reverses nesfatin‐1 activities of reducing ER stress and attenuating MI/R injury. (A‐E) Mice were administrated intramyocardially with 10 ng/g bodyweight nesfatin‐1 combined with or without 1 μg/g bodyweight wortmannin at 30 min after ischaemia. Each group contains seven mice. (A) The protein expression of p‐Akt, Akt, p‐ERK, ERK, CHOP, ATF6, GPR78 and caspase‐12 in heart homogenates was determined by Western blotting analysis. Images are representative of three independent experiments. (B) Infarct area in the heart slices was evaluated by TTC staining. (C) Plasma cardiac troponin T level in the serum was assessed using ELISA assay. (D) Myocardial apoptosis was detected by TUNEL staining, and the percentage of apoptotic myocardial cells is depicted on the right. (E) The caspase‐3 activity in heart homogenates was determined by caspase activity assay. Data are mean ± SD (7). Student's t test. *, P < .05; **, P < .01; NS, not significant
Article Snippet: The activity of caspase‐3 was detected by Caspase‐3 Activity Assay Kit (#5723, Cell Signaling Technology), and the LDH activity was assessed by the
Techniques: Inhibition, Expressing, Western Blot, Staining, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, TUNEL Assay, Activity Assay, Caspase Activity Assay
Journal: Journal of Biochemical and Molecular Toxicology
Article Title: Bradykinin/bradykinin 1 receptor promotes brain microvascular endothelial cell permeability and proinflammatory cytokine release by downregulating Wnt3a
doi: 10.1002/jbt.23213
Figure Lengend Snippet: BK enhanced ROS production, cellular permeability, and inflammation, and reduced cell proliferation and tight junction formation by BMECs. BMECs were treated with BK (low concentration, 100 nM or high concentration, 400 nM). ROS production was determined by flow cytometry, and the respective images are shown (A, left panel). Summarized results from three independent experiments are shown (A, right panel). Cell permeability was tested by sodium fluorescein analysis (B, left panel) and the lucifer yellow assay (B, right panel). Cell proliferation was measured by EdU staining. (C, IL‐6, MCP‐1, and IL‐18 expressions were detected by IF (D) and ELISA (E). (F) The cell apoptosis rate was measured using FCM. (G) LDH levels were determined by ELISA. The levels of claudin‐5, occludin, β‐catenin, Wnt3a, and B1R expression were determined by western blotting (H, left panel). The statistical results of western blot studies conducted in three independent experiments (H, right panel). * p < 0.05; ** p < 0.01; *** p < 0.001 versus blank. B1R, bradykinin 1 receptor; BK, bradykinin; BMECs, brain microvascular endothelial cells; DCF‐A, 2′,7′‐dichlorodihydrofluorescein diacetate; EdU, 5‐ethynyl‐2′‐deoxyuridine; ELISA, enzyme‐linked Immunosorbent assay; FCM, flow cytometry; GAPDH glyceraldehyde‐3‐phosphate dehydrogenase; IF, immunofluorescence; IL‐6, interleukin 6; LDH, lactate dehydrogenase; MCP‐1, monocyte chemoattractant protein‐1; ROS, reactive oxygen species.
Article Snippet: The levels of IL‐6 (Elabscience; Cat. No. E‐EL‐H0102c), IL‐18 (Boster; CAT. No. EK0864), MCP‐1 (Boster; Cat. No. EK0441), and
Techniques: Permeability, Concentration Assay, Flow Cytometry, Staining, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot, Immunofluorescence
Journal: Journal of Biochemical and Molecular Toxicology
Article Title: Bradykinin/bradykinin 1 receptor promotes brain microvascular endothelial cell permeability and proinflammatory cytokine release by downregulating Wnt3a
doi: 10.1002/jbt.23213
Figure Lengend Snippet: Wnt3a counteracted the effects of BK on BMECs. BMECs were treated with a high concentration (400 nM) of BK or a high concentration of both BK and Wnt3a (100 ng/ml each). ROS production was measured by flow cytometry, and the respective images are shown (A, left panel). The summary results of three independent experiments are shown (A, right panel). Cell permeability was tested by sodium fluorescein analysis (B, left panel) and the lucifer yellow assay (B, right panel). (C) Cell proliferation was measured by EdU staining. IL‐6, MCP‐1, and IL‐18 expressions were detected by (D) IF and (E) ELISA. (F) Cell apoptosis was detected by using the FCM method. (G) LDH levels were determined by ELISA. The levels of claudin‐5, occludin, β‐catenin, Wnt3a, and B1R expression were determined by western blotting (H, left panel). The statistical results of western blot studies conducted in three independent experiments (H, right panel). * p < 0.05; ** p < 0.01; *** p < 0.001 versus blank. # p < 0.05; ## p < 0.01 versus BK‐high. B1R, bradykinin 1 receptor; BK, bradykinin; BMECs, brain microvascular endothelial cells; DCF‐A, 2′,7′‐dichlorodihydrofluorescein diacetate; EdU, 5‐ethynyl‐2′‐deoxyuridine; ELISA, enzyme‐linked Immunosorbent assay; FCM, flow cytometry; GAPDH glyceraldehyde‐3‐phosphate dehydrogenase; IF, immunofluorescence; IL‐6, interleukin 6; LDH, lactate dehydrogenase; MCP‐1, monocyte chemoattractant protein‐1; ROS, reactive oxygen species.
Article Snippet: The levels of IL‐6 (Elabscience; Cat. No. E‐EL‐H0102c), IL‐18 (Boster; CAT. No. EK0864), MCP‐1 (Boster; Cat. No. EK0441), and
Techniques: Concentration Assay, Flow Cytometry, Permeability, Staining, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot, Immunofluorescence
Journal: Nutrients
Article Title: Effects of Co-Ingestion of β-Hydroxy-β-Methylbutyrate and L-Arginine α-Ketoglutarate on Jump Performance in Young Track and Field Athletes
doi: 10.3390/nu13041064
Figure Lengend Snippet: Lactate dehydrogenase (LDH) concentration in subsequent days in SUP and PL groups (* significant change ( p < 0.05) to baseline in PL group; # significant change ( p < 0.05) to baseline in SUP group).
Article Snippet: CK and LDH tests were performed in a laboratory that validated methods for the determination of these particles using biochemical tests (i-STAT ® CK-MB (Abbott, Chicago, IL, USA) (biological material—blood serum, analytical sensitivity ≤ 0.1 ng/mL), and
Techniques: Concentration Assay