Journal: Pharmaceuticals

Article Title: Tocotrienol-Rich Fraction Ameliorates the Aluminium Chloride-Induced Neurovascular Dysfunction-Associated Vascular Dementia in Rats

doi: 10.3390/ph16060828

Figure Lengend Snippet: Microscopic images representing immunohistochemical staining of PDGF-C expression in the hippocampus (upper panel 40× magnification; scale bar 500 µm) and its corresponding CA1 area (lower panel 200× magnification; scale bar 100 µm). The high-magnification images in the lower panel indicate PDGF-C expression in the CA1 area. The PDGF-C expression is strongly positive in the CON group rats, faintly positive in the AlCl 3 and TRF 30 group rats, mid-positive in the TRF 60 and TRF 120 group rats, and strongly positive in the DON group rats. Abbreviations: AlCl 3 , aluminium chloride; CA1, cornu ammonis 1; CON, control; DON, donepezil; PDGF-C, platelet-derived growth factor-C; and TRF, tocotrienol-rich fraction.

Article Snippet: AlCl 3 (Friendemann Schmidt Chemical, Malaysia), myeloperoxidase activity assay kit (Elabscience Biotechnology Inc., Houston, TX, USA), nitrite assay kit (Sigma-Aldrich, St. Louis, MO, USA), rabbit polyclonal against platelet-derived growth factor C (Abbexa, Cambridge, UK) and rabbit specific HRP_DAB IHC detection kit—micro-polymer v2d, ab236469 (Abcam, Waltham/Boston, MA, USA) were used.

Techniques: Immunohistochemical staining, Staining, Expressing, Control, Derivative Assay

Journal: bioRxiv

Article Title: Corilagin controls post-parasiticide schistosome egg-induced liver fibrosis by inhibiting Stat6 signalling pathway

doi: 10.1101/340299

Figure Lengend Snippet: Effect of Corilagin on the expression of ARG1 according to ELISA. Data shown are the mean ± SD from 3 independent experiments. # P< 0.05 vs . normal group; *P< 0.05 VS model group; as determined by Student’s t-test; ## P< 0.01 determined by One-way ANOVA.

Article Snippet: The Mouse ARG1, Fizz1, Ym1, TGFβ and PDGF ELISA kits were purchased from Elabscience Biotechnology Co., Ltd (Wuhan, China).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Journal: bioRxiv

Article Title: Corilagin controls post-parasiticide schistosome egg-induced liver fibrosis by inhibiting Stat6 signalling pathway

doi: 10.1101/340299

Figure Lengend Snippet: Effect of Corilagin on expression of PDGF, Fizz1, Ym1, and TGFβ according to ELISA. Data shown are the mean ± SD from 6 experiment mice. # P< 0.05, ## P< 0.01 vs . normal group; *P< 0.05, ** P< 0.01 VS model group; As determined by Student’s t-test; ### P< 0.01 determined by One-way ANOVA.

Article Snippet: The Mouse ARG1, Fizz1, Ym1, TGFβ and PDGF ELISA kits were purchased from Elabscience Biotechnology Co., Ltd (Wuhan, China).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Journal: Journal of Translational Medicine

Article Title: Papillary thyroid cancer organoids harboring BRAF V600E mutation reveal potentially beneficial effects of BRAF inhibitor-based combination therapies

doi: 10.1186/s12967-022-03848-z

Figure Lengend Snippet: List of drugs used in this study

Article Snippet: VEGFR, PDGFRβ , Lenvatinib , MedChemExpress , HY-10981 , 10.

Techniques: DNA Synthesis

Journal: Journal of experimental & clinical cancer research : CR

Article Title: Chemotherapy-elicited extracellular vesicle CXCL1 from dying cells promotes triple-negative breast cancer metastasis by activating TAM/PD-L1 signaling.

doi: 10.1186/s13046-024-03050-7

Figure Lengend Snippet: Fig. 3 EV-dead promotes the invasion and BCSC subpopulation of the co-cultured human TNBC MDA-MB-231 cells by inducing macrophage M2 polarization. A Diagram of the EV-deadADR and EV-alive-H separation procedures and their representative TEM images. Scale bar: 100 nm. B EV protein markers were identified by Western blotting; (C) EV sizes and concentrations were detected by NTA analysis; (D) CXCL1 concentrations in EV-deadADR and EV-alive-H were detected by an ELISA assay; (E, F) The polarization changes of THP1 macrophages after EV-deadADR treatment (25–100 μg/ml) for 48 h; 50 μg/ml EV-dead was used for the Western blotting assay; G Invasion efficacy changes of the co-cultured MDA-MB-231 cells after EV-deadADR treatment as indicated. Scale bars: 100 μm; H Changes in apoptosis resistance of the co-cultured MDA-MB-231 cells to paclitaxel after EV-deadADR treatment for 48 h, as determined by annexin V-FITC/PI staining and flow cytometry; I The ALDH+ BCSC subpopulation and CD133+ BCSC subpopulation in the co-cultured MDA-MB-231 cells after EV-deadADR treatment for 48 h were detected by flow cytometry; n = 3. Data are presented as mean ± SD. *p < 0.05, **p < 0.01

Article Snippet: As CXCL1 is a chemokine, the commercialized Chemokine Inhibitor Compound Library (TargetMol, Catalog Number: L7600) containing 80 small molecule compounds was screened by ELISA (Fig. 8A).

Techniques: Cell Culture, Western Blot, Enzyme-linked Immunosorbent Assay, Staining, Flow Cytometry

Journal: Journal of experimental & clinical cancer research : CR

Article Title: Chemotherapy-elicited extracellular vesicle CXCL1 from dying cells promotes triple-negative breast cancer metastasis by activating TAM/PD-L1 signaling.

doi: 10.1186/s13046-024-03050-7

Figure Lengend Snippet: Fig. 4 CXCL1EV-dead induces macrophage M2 polarization by activating PD-L1 expression. A Chemokine array assay was conducted to characterize the differences in chemokine content between EV-dead and EV-alive. An ELISA assay was conducted to compare the relative CXCL1 content in EV-dead and EV-alive. B Changes in M2 phenotype polarization of Raw264.7 macrophages when treated with 10 ng/ml murine CXCL1, 50 μg/ ml EV-dead, 50 μg/ml EV-deadshCXCL1, 5 μg/ml CXCL1 neutralizing antibody (NA), or EV-dead and CXCL1-NA combination for 48 h. C Representative images of Transwell assay. Raw264.7 macrophages were treated as indicated for 48 h and then co-cultured with 4 T1 cells. Scale bar: 200 μm. D–F Expression changes of CXCL1 and PD-L1 in Raw264.7 macrophages when treated as indicated for 48 h. Scale bar: 10 μm. G The results of the flow cytometry assay suggested that 50 μg/ml EV-dead treatment for 48 h induced the M2 polarization of Raw264.7 macrophages by activating PD-L1 expression; n = 3. Data are presented as mean ± SD. *p < 0.05, **p < 0.01

Article Snippet: As CXCL1 is a chemokine, the commercialized Chemokine Inhibitor Compound Library (TargetMol, Catalog Number: L7600) containing 80 small molecule compounds was screened by ELISA (Fig. 8A).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Transwell Assay, Cell Culture, Flow Cytometry

Journal: Journal of experimental & clinical cancer research : CR

Article Title: Chemotherapy-elicited extracellular vesicle CXCL1 from dying cells promotes triple-negative breast cancer metastasis by activating TAM/PD-L1 signaling.

doi: 10.1186/s13046-024-03050-7

Figure Lengend Snippet: Fig. 5 CXCL1EV-dead promotes TNBC growth and lung metastasis in vivo by activating TAM/PD-L1 signaling. A The successful generation of 4 T1/rCXCL1Flag cells was validated by immunoblotting and immunofluorescence assays. Scale bar: 5 μm. B The difference in CXCL1 content between EV-dead and EV-deadrCXCL1-Flag was compared by ELISA. EV-deadrCXCL1-Flag was isolated from the supernatants of apoptotic 4 T1/rCXCL1Flag cells induced by paclitaxel treatment; n = 3. C, D Peritumoral injection with EV-deadrCXCL1 (200 μg/20 g weight, q3d) significantly accelerated TNBC growth (C) and lung metastasis (D) compared to that of the EV-dead group (200 μg/20 g weight, q3d); Tumor volume: n = 6; Number of metastatic lesions, n = 3; K-M curves of lung metastasis time, n = 10. Scale bar: 1 cm. E Tumor tissue immunofluorescence experiment showed that flag-tagged CXCL1 (red) from EV-deadrCXCL1-Flag was predominantly phagocytosed by CD206+ macrophages (green) in the TME. Scale bar: 5 μm. F The infiltration levels of CD45+/F4/80+/CD206+ TAMs (up) and CD45+/F4/80+/PD-L1+ TAMs (down) in the TME of mice following treatment with saline, EV-dead, or EV-deadrCXCL1-Flag; n = 3. G QPCR assay was conducted to investigate the CTC quantity in the peripheral blood of mice following treatment with saline, EV-dead, or EV-deadrCXCL1-Flag; n = 3. Data are presented as mean ± SD. *p < 0.05, **p < 0.01

Article Snippet: As CXCL1 is a chemokine, the commercialized Chemokine Inhibitor Compound Library (TargetMol, Catalog Number: L7600) containing 80 small molecule compounds was screened by ELISA (Fig. 8A).

Techniques: In Vivo, Western Blot, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Isolation, Injection, Saline

Journal: Journal of experimental & clinical cancer research : CR

Article Title: Chemotherapy-elicited extracellular vesicle CXCL1 from dying cells promotes triple-negative breast cancer metastasis by activating TAM/PD-L1 signaling.

doi: 10.1186/s13046-024-03050-7

Figure Lengend Snippet: Fig. 6 CXCL1 knockdown in EV-dead or macrophage depletion inhibits EV-dead-induced TNBC growth and lung metastasis in vivo. A The successful generation of 4 T1/shCXCL1 cells was verified by western blotting assay. The difference in CXCL1 content between EV-dead and EV-deadshCXCL1 was compared by ELISA. EV-deadshCXCL1 was isolated from the supernatants of apoptotic 4 T1/shCXCL1 cells induced by paclitaxel treatment; n = 3. B Representative images of the tumors (n = 7) and the in vivo imaging assay (n = 3), and mouse weight and tumor volume curves (n = 7). Clodronate liposomes (CL) were used to deplete macrophages in the TME of the 4 T1-Luc xenograft model. Scale bar: 2 cm. C Representative images of the lungs (n = 3) and lung HE assay (n = 3) as well as the K-M curves of lung metastasis time (n = 10). Scale bar: 100 μm. D, E The infiltration levels of CD45+/F4/80+/CD206+ TAMs (D) and CD45+/F4/80+/PD-L1+ TAMs (E) in the TME of mice following treatment with EV-dead, EV-deadshCXCL1, or the combination of EV-dead and CL; n = 3. F CD206 (green) and PD-L1 (red) expression levels in the TME. Arrows indicate PD-L1 expression in TAMs. Scale bar: 10 μm. G The quantity of CTCs in the peripheral blood of mice treated as indicated; n = 3. Data are presented as mean ± SD. *p < 0.05, **p < 0.01

Article Snippet: As CXCL1 is a chemokine, the commercialized Chemokine Inhibitor Compound Library (TargetMol, Catalog Number: L7600) containing 80 small molecule compounds was screened by ELISA (Fig. 8A).

Techniques: Knockdown, In Vivo, Western Blot, Enzyme-linked Immunosorbent Assay, Isolation, In Vivo Imaging, Liposomes, Expressing

Journal: Journal of experimental & clinical cancer research : CR

Article Title: Chemotherapy-elicited extracellular vesicle CXCL1 from dying cells promotes triple-negative breast cancer metastasis by activating TAM/PD-L1 signaling.

doi: 10.1186/s13046-024-03050-7

Figure Lengend Snippet: Fig. 7 CXCL1EV-dead transcriptionally increases PD-L1 expression in macrophages by activating EED signaling. A The mRNA level of PD-L1 in Raw264.7 macrophages was significantly increased by 10 ng/ml murine CXCL1 and 50 μg/ml EV-dead treatment for 24 h; (B) The promoter activity of PD-L1 in Raw264.7 cells when treated as indicated for 24 h; CXCL1-NA concentration: 5 μg/ml; (C) Diagram of the DNA-pull down-MS assay. The DEPs that bind with the PD-L1 promoter region of Raw264.7 macrophages after CXCL1 treatment for 24 h were analyzed by mass spectrometry. The TFs of PD-L1 were predicted using the hTFtarget database. EED was selected as the potential transcription factor by taking the intersection of the DEP set and the TF set. D, E The expression levels of EED and PD-L1 in Raw264.7 cells when treated as indicated for 48 h. Murine CXCL1 concentration: 10 ng/ml. Scale bar: 5 μm. F The combinational effect of CXCL1 treatment and EED knockdown on the promoter activity of PD-L1 in Raw264.7 cells when treated as indicated for 24 h; (G) The binding activity of EED with the promoter fragment of PD-L1 in Raw264.7 cells when treated as indicated for 48 h was investigated by CHIP-PCR assay. H The antisense mutation of the EED binding region in the PD-L1 promoter significantly abrogated the induction effect of CXCL1 on PD-L1 promoter activity in Raw264.7 macrophages; n = 3. Data are presented as mean ± SD. *p < 0.05, **p < 0.01

Article Snippet: As CXCL1 is a chemokine, the commercialized Chemokine Inhibitor Compound Library (TargetMol, Catalog Number: L7600) containing 80 small molecule compounds was screened by ELISA (Fig. 8A).

Techniques: Expressing, Activity Assay, Concentration Assay, Mass Spectrometry, Knockdown, Binding Assay, Mutagenesis

Journal: Journal of experimental & clinical cancer research : CR

Article Title: Chemotherapy-elicited extracellular vesicle CXCL1 from dying cells promotes triple-negative breast cancer metastasis by activating TAM/PD-L1 signaling.

doi: 10.1186/s13046-024-03050-7

Figure Lengend Snippet: Fig. 8 TPCA-1 significantly inhibits CXCL1EV-dead-EV-dead-induced chemoresistance and invasion of TNBC cells co-cultured with macrophages. A, B Diagram of the CXCL1 secretion inhibitor screening assay. 4 T1 cells were treated with 80 kinds of compounds (1 μM) for 48 h, and the top five compounds with the strongest inhibitory activities on CXCL1 secretion of 4 T1 cells were selected; n = 3. C, D The cytotoxicity of TPCA-1 in TNBC 4 T1 cells (n = 8) and its effect on the apoptosis resistance of 4 T1 cells to paclitaxel (n = 3). Cells were treated as indicated for 48 h. E–G TPCA-1 treatment for 48 h had no significant effect on EV-dead secretion (E) from 4 T1 cells but significantly attenuated the concentration of CXCL1 in the supernatants of 4 T1 cells (F) and the EV-dead of apoptotic 4 T1 cells (G); n = 3. H The results of the flow cytometry assay indicated that 1 μM TPCA-1 treatment for 48 h significantly reversed the induction effect of EV-dead (50 μg/ml) on the M2 polarization of macrophages; n = 3. I, J Apoptosis and Transwell assays suggested that TPCA-1 treatment (1 μM) for 48 h inhibited 50 μg/ml EV-dead-induced apoptosis resistance (n = 3) and invasion (n = 3) of 4 T1 cells in the co-culture system; Scale bar: 100 μm. Data are presented as mean ± SD. *p < 0.05, **p < 0.01

Article Snippet: As CXCL1 is a chemokine, the commercialized Chemokine Inhibitor Compound Library (TargetMol, Catalog Number: L7600) containing 80 small molecule compounds was screened by ELISA (Fig. 8A).

Techniques: Cell Culture, Screening Assay, Concentration Assay, Flow Cytometry, Co-Culture Assay

Journal: Theranostics

Article Title: Meningeal macrophages regulate fibroblasts to influence meningeal lymphatic function following traumatic brain injury

doi: 10.7150/thno.130263

Figure Lengend Snippet: PDGF-C enhances VEGF-C production by meningeal fibroblasts and promotes the recovery of meningeal lymphatic function after TBI. (A) Schematic of the signaling network through which other cell types regulate meningeal fibroblasts. (B) Dot plot showing macrophage-fibroblast interactions through ligand-receptor pairs, quantified by ligand-receptor scores. (C) Pdgfc/Pdgfra signaling network from other cells to fibroblasts. (D) Violin plots showing the expression levels of Pdgfc across cell types. (E) Violin plots showing the expression levels of Pdgfc in macrophage subsets. (F) Immunofluorescence staining showed colocalization of PDGF-C with macrophages (CD206). (G) ELISA analysis showing PDGF-C levels after TBI and macrophage depletion (n = 5). (H) Experimental design for TBI and uninjured mice with subdural injection of PDGF-C or vehicle. (I) Representative flow cytometry plots and quantification of CD45⁻CD31⁻VEGF-C⁺ cells from TBI mice following subdural injection of PDGF-C or vehicle (n = 5). (J) Immunofluorescence showing mLVs (LYVE-1) and VEGF-C⁺ cells in the meninges of TBI mice after subdural injection of PDGF-C or vehicle and quantification of LYVE-1 coverage, and VEGF-C⁺ cell abundance in these two groups (n = 4). (K) Representative images and quantification of fluorescent beads accumulation in hot spots (n = 4). (L) Representative images and quantification of fluorescent beads accumulation in dCLNs (n = 6 for TBI + Vehicle, n = 5 for TBI + PDGF-C). (M) Representative flow cytometry plots and quantification of the proportion of VEGF-C⁺ cells in NIH/3T3 fibroblasts treated with different concentrations of PDGF-C in vitro (n = 5). (N) Representative images and quantification of VEGF-C⁺ cells in NIH/3T3 fibroblasts treated with different concentrations of PDGF-C in vitro (n = 9). (O) Timeline of experimental design illustrating the viral delivery and TBI induction. (P) Representative immunofluorescence images and quantification showing the number of VEGF-C⁺ cells and LYVE-1 coverage in meninges isolated from TBI mice following AAV9 treatment (n = 4).

Article Snippet: An external injection needle was then repeatedly inserted through the cannula into the subdural space, allowing multiple administrations of PDGF-C (0.1 μg/μL, HY- P73354 , MCE) over several days while minimizing tissue damage from repeated operations.

Techniques: Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Injection, Flow Cytometry, In Vitro, Isolation

Journal: Theranostics

Article Title: Meningeal macrophages regulate fibroblasts to influence meningeal lymphatic function following traumatic brain injury

doi: 10.7150/thno.130263

Figure Lengend Snippet: PDGF - C - mediated recovery of meningeal lymphatic function improves post - TBI neuroinflammation and neurological outcomes . (A) Sensorimotor function assessment in TBI + Vehicle, TBI + PDGF-C, Vehicle, and PDGF-C groups at 3, 5, and 7 days post-TBI using the adhesive removal test, cylinder test, and foot fault test (n = 10 for TBI + Vehicle and TBI + PDGF-C groups; n = 6 for Vehicle and PDGF-C groups). (B) Changes in the proportion and number of infiltrating lymphoid cells within the injured hemisphere (n = 5). (C, D) Representative images and quantification of MBP and SMI32 coverage in the injured hemisphere at 7 days post-TBI (n = 5). (E, F) Representative images and quantification of activated microglia (CD68⁺IBA-1⁺) in the cortex, dentate gyrus of hippocampus and striatum (n = 5). (G, H) Representative images and quantification of GFAP (green) coverage in the injured hemisphere (n = 5). (I) Experimental design for long-term memory and cognitive assessment in TBI + PDGF-C and TBI + Vehicle groups at 28 days post-TBI (n = 10) (J) Representative path tracings during the probe trial, and quantification of swimming speed, escape latency, platform crossings, and time spent in target quadrant in Morris water maze test (n = 10). * TBI + vehicle vs. sham; # TBI + PDGF-C vs. TBI + vehicle. (K, L) Schematic and representative heatmaps during testing, and quantification of time spent in the novel arms in Y-maze test (n = 10). (M) Schematic and quantification of the recognition ratio in the novel object recognition test (n = 10). * P < 0.05, ** P < 0.01, # P < 0.05.

Article Snippet: An external injection needle was then repeatedly inserted through the cannula into the subdural space, allowing multiple administrations of PDGF-C (0.1 μg/μL, HY- P73354 , MCE) over several days while minimizing tissue damage from repeated operations.

Techniques: Adhesive

Journal: Pharmacological research

Article Title: Remote ischemic conditioning attenuates blood-brain barrier disruption after recombinant tissue plasminogen activator treatment via reducing PDGF-CC.

doi: 10.1016/j.phrs.2022.106641

Figure Lengend Snippet: Fig. 4. RIPreC attenuated the phosphorylation of PDGFRα in ischemic brain tissue by reducing the blood levels of PDGF-CC. (A-C) Western blot and quantification of phosphorylated and total PDGFRα in ischemic penumbra cortex at 24 h after intravenous thrombolysis (n = 6 rats per group). Three representative samples were shown. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (D) ELISA analysis of serum PDGF-CC at 24 h after intravenous thrombolysis. (n = 6–9 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures before stroke. * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (E) The schematic protocol for healthy rats receiving RIC treatment. Serum samples were collected at day 0 (baseline), day 1, day 7 of RIC, and 24 h after the last RIC procedure (day 8). (F) ELISA analysis of serum PDGF-CC in non-stroke rats after RIC or sham-operation (n = 8 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPreC rats received both procedures. ** P < 0.01, * ** P < 0.001, two-way ANOVA. Data represent mean ± SEM. (G) The schematic protocol for healthy humans receiving 7-day RIC treatment. (H-I) ELISA analysis of serum PDGF-CC levels in 30 healthy humans. One-way ANOVA. Data represent mean ± SEM.

Article Snippet: The rat PDGF-CC protein level was measured using a rat PDGF-CC ELISA kit (CSB-EL017710RA; Cusabio, Houston, TX, USA).

Techniques: Phospho-proteomics, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Pharmacological research

Article Title: Remote ischemic conditioning attenuates blood-brain barrier disruption after recombinant tissue plasminogen activator treatment via reducing PDGF-CC.

doi: 10.1016/j.phrs.2022.106641

Figure Lengend Snippet: Fig. 6. RIC reduces circulating PDGF-CC levels by reducing the PDGF-CC level in the skeletal muscle from RIC-treated hindlimbs and blood platelets. (A-C) Western blot and qRT-PCR analysis of Hif-1α levels in the hindlimbs skeletal muscles receiving RIC or sham procedure. Healthy rats received RIC or sham operation for 7 days and the skeletal muscles from the treated hindlimbs were harvested 24 h after the last round of RIC. Three representative samples were shown (n = 6 rats per group). * P < 0.05, unpaired t-test. Data represent mean ± SEM. (D-F) Western blot analysis of PDGF-CC levels in the skeletal muscles of the hindlimbs receiving RIC or sham procedure (n = 8 rats per group). Three representative samples were shown. Unpaired t-test, * ** P < 0.001. Data represent mean ± SEM. (G-H) ELISA and qRT-PCR analysis of PDGF-CC protein and Pdgfc mRNA levels in the hindlimbs skeletal muscles receiving RIC or sham procedure (n = 8 rats per group) * P < 0.05, * * P < 0.01, unpaired t-test. Data represent mean ± SEM. (I-J) Platelets analysis from blood routine examination in rats received RIC or sham procedure. The blood samples were obtained via inferior vena cava of rats which received a 7-day RIC or sham operation (n = 9 rats per group). Unpaired t-test, * P < 0.05. Data represent mean ± SEM. (K-L) ELISA analysis of PDGF-CC level from platelets or plasma in healthy rats after RIC or sham operation (n = 10 rats per group). Unpaired t-test, * P < 0⋅05. Data represent mean ± SEM. (M) ELISA analysis of PDGF-CC level from indicated tissues harvested from healthy rats after RIC or sham operation (n = 6 rats per group). * ** P < 0.001, Unpaired t-test. Data represent mean ± SEM.

Article Snippet: The rat PDGF-CC protein level was measured using a rat PDGF-CC ELISA kit (CSB-EL017710RA; Cusabio, Houston, TX, USA).

Techniques: Western Blot, Quantitative RT-PCR, Muscles, Enzyme-linked Immunosorbent Assay, Clinical Proteomics

Journal: Pharmacological research

Article Title: Remote ischemic conditioning attenuates blood-brain barrier disruption after recombinant tissue plasminogen activator treatment via reducing PDGF-CC.

doi: 10.1016/j.phrs.2022.106641

Figure Lengend Snippet: Fig. 7. The protective effect of RIPostC on BBB integrity was also dependent on reduction of the blood PDGF-CC levels. (A) The schematic protocol for RIPostC intervention in rats with embolic stroke. (B-C) Representative images of TTC staining at 72 h after intravenous thrombolysis (n = 8 rats per group). Sham rats received only anesthesia without RIC procedure, while RIPostC rats received both procedures after thrombolysis. * P < 0.05, unpaired t-test. Data represent mean ± SEM. (D) Neurological deficit score at 1 and 3 days after intravenous thrombolysis (n = 10 rats per group). * P < 0.05, two-way ANOVA. Data represent mean ± SEM. (E) qRT-PCR analysis of IL-1β, IL-6, and TNF-α mRNA levels. (n = 8 rats per group). * * P < 0.01, * ** P < 0.001, unpaired t-test. Data represent mean ± SEM. (F) ELISA analysis of serum PDGF-CC (n = 10 rats per group). * * P < 0.01, two-way ANOVA. Data represent mean ± SEM. (G-H) Evans blue leakage at 72 h post intravenous thrombolysis. Recombinant PDGF-CC or normal saline were intravenously injected before and at 24 h and 48 h after thrombolysis (n = 9 rats per group). * P < 0.05, * * P < 0.01, one-way ANOVA. Data represent mean ± SEM. (I-J) The schematic protocol and ELISA analysis for RIPostC intervention in AIS patients with intravenous thrombolysis. Participants received two administrations of RIPostC (22 patients) or sham (20 patients) treatment at 6 h for the first round and 18 h for the second round after intravenous thrombolysis. Unpaired t-test. Data represent mean ± SEM.

Article Snippet: The rat PDGF-CC protein level was measured using a rat PDGF-CC ELISA kit (CSB-EL017710RA; Cusabio, Houston, TX, USA).

Techniques: Staining, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Recombinant, Saline, Injection