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OSC hindered the adhesion and F-actin polymerization in the H37Rv-infected neutrophils by the inhibition of the TLR2/MyD88/Src/ERK1/2 signaling pathway. A-C. The neutrophils were uninfected or infected with H37Rv (5 MOI) in the presence or absence of 5 μM OSC. A. The firmly adherent neutrophils were counted after the H37Rv infection for 6, 12, 18, and 24 h. B. F-actin polymerization was monitored using immunofluorescent microscopy at 24 h after the H37Rv infection. C. A Western blot analysis was performed to assess the expressions of TLR2, MyD88, Src, p-ERK1/2, ERK1/2, p-p38 MAPK, p38 MAPK, p-JNK, and JNK at 24 h after the H37Rv infection. β-actin was used as an endogenous control. D and E. The neutrophils were preincubated with the Src kinase inhibitor <t>PP1</t> (5 μM), ERK1/2 inhibitor U0126 (10 μM), p38MAPK inhibitor SB202190 (10 μM), or the JNK inhibitor AG490 (25 μM) for 30 min or pretransfected with siTLR2 (100 nM) for 24 h, and then uninfected or infected with H37Rv (5 MOI) in the presence or absence of OSC (5 μM) for 24 h. D. The firmly adherent neutrophils were counted. E. F-actin polymerization was monitored. Data are expressed as the mean ± SD of the three independent experiments. *P < 0.05, **P < 0.01 compared with Ctrl group. #P < 0.05 compared with the Mtb group. Ctrl: control; OSC: Oxysophocarpine; NS: no significance.
Src Kinase Inhibitor Pp1, supplied by Biomol GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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the src family kinase inhibitor pp1  (Millipore)
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OSC hindered the adhesion and F-actin polymerization in the H37Rv-infected neutrophils by the inhibition of the TLR2/MyD88/Src/ERK1/2 signaling pathway. A-C. The neutrophils were uninfected or infected with H37Rv (5 MOI) in the presence or absence of 5 μM OSC. A. The firmly adherent neutrophils were counted after the H37Rv infection for 6, 12, 18, and 24 h. B. F-actin polymerization was monitored using immunofluorescent microscopy at 24 h after the H37Rv infection. C. A Western blot analysis was performed to assess the expressions of TLR2, MyD88, Src, p-ERK1/2, ERK1/2, p-p38 MAPK, p38 MAPK, p-JNK, and JNK at 24 h after the H37Rv infection. β-actin was used as an endogenous control. D and E. The neutrophils were preincubated with the Src kinase inhibitor <t>PP1</t> (5 μM), ERK1/2 inhibitor U0126 (10 μM), p38MAPK inhibitor SB202190 (10 μM), or the JNK inhibitor AG490 (25 μM) for 30 min or pretransfected with siTLR2 (100 nM) for 24 h, and then uninfected or infected with H37Rv (5 MOI) in the presence or absence of OSC (5 μM) for 24 h. D. The firmly adherent neutrophils were counted. E. F-actin polymerization was monitored. Data are expressed as the mean ± SD of the three independent experiments. *P < 0.05, **P < 0.01 compared with Ctrl group. #P < 0.05 compared with the Mtb group. Ctrl: control; OSC: Oxysophocarpine; NS: no significance.
The Src Family Kinase Inhibitor Pp1, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/the src family kinase inhibitor pp1/product/Millipore
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the src family kinase inhibitor pp1 - by Bioz Stars, 2026-03
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src kinase-specific inhibitor pp1  (Biomol GmbH)
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OSC hindered the adhesion and F-actin polymerization in the H37Rv-infected neutrophils by the inhibition of the TLR2/MyD88/Src/ERK1/2 signaling pathway. A-C. The neutrophils were uninfected or infected with H37Rv (5 MOI) in the presence or absence of 5 μM OSC. A. The firmly adherent neutrophils were counted after the H37Rv infection for 6, 12, 18, and 24 h. B. F-actin polymerization was monitored using immunofluorescent microscopy at 24 h after the H37Rv infection. C. A Western blot analysis was performed to assess the expressions of TLR2, MyD88, Src, p-ERK1/2, ERK1/2, p-p38 MAPK, p38 MAPK, p-JNK, and JNK at 24 h after the H37Rv infection. β-actin was used as an endogenous control. D and E. The neutrophils were preincubated with the Src kinase inhibitor <t>PP1</t> (5 μM), ERK1/2 inhibitor U0126 (10 μM), p38MAPK inhibitor SB202190 (10 μM), or the JNK inhibitor AG490 (25 μM) for 30 min or pretransfected with siTLR2 (100 nM) for 24 h, and then uninfected or infected with H37Rv (5 MOI) in the presence or absence of OSC (5 μM) for 24 h. D. The firmly adherent neutrophils were counted. E. F-actin polymerization was monitored. Data are expressed as the mean ± SD of the three independent experiments. *P < 0.05, **P < 0.01 compared with Ctrl group. #P < 0.05 compared with the Mtb group. Ctrl: control; OSC: Oxysophocarpine; NS: no significance.
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https://www.bioz.com/result/src kinase-specific inhibitor pp1/product/Biomol GmbH
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src kinase-specific inhibitor pp1 - by Bioz Stars, 2026-03
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selective inhibitor src family tyrosine kinases, pp1  (Tocris)
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Tocris selective inhibitor src family tyrosine kinases, pp1
OSC hindered the adhesion and F-actin polymerization in the H37Rv-infected neutrophils by the inhibition of the TLR2/MyD88/Src/ERK1/2 signaling pathway. A-C. The neutrophils were uninfected or infected with H37Rv (5 MOI) in the presence or absence of 5 μM OSC. A. The firmly adherent neutrophils were counted after the H37Rv infection for 6, 12, 18, and 24 h. B. F-actin polymerization was monitored using immunofluorescent microscopy at 24 h after the H37Rv infection. C. A Western blot analysis was performed to assess the expressions of TLR2, MyD88, Src, p-ERK1/2, ERK1/2, p-p38 MAPK, p38 MAPK, p-JNK, and JNK at 24 h after the H37Rv infection. β-actin was used as an endogenous control. D and E. The neutrophils were preincubated with the Src kinase inhibitor <t>PP1</t> (5 μM), ERK1/2 inhibitor U0126 (10 μM), p38MAPK inhibitor SB202190 (10 μM), or the JNK inhibitor AG490 (25 μM) for 30 min or pretransfected with siTLR2 (100 nM) for 24 h, and then uninfected or infected with H37Rv (5 MOI) in the presence or absence of OSC (5 μM) for 24 h. D. The firmly adherent neutrophils were counted. E. F-actin polymerization was monitored. Data are expressed as the mean ± SD of the three independent experiments. *P < 0.05, **P < 0.01 compared with Ctrl group. #P < 0.05 compared with the Mtb group. Ctrl: control; OSC: Oxysophocarpine; NS: no significance.
Selective Inhibitor Src Family Tyrosine Kinases, Pp1, supplied by Tocris, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/selective inhibitor src family tyrosine kinases, pp1/product/Tocris
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selective inhibitor src family tyrosine kinases, pp1 - by Bioz Stars, 2026-03
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OSC hindered the adhesion and F-actin polymerization in the H37Rv-infected neutrophils by the inhibition of the TLR2/MyD88/Src/ERK1/2 signaling pathway. A-C. The neutrophils were uninfected or infected with H37Rv (5 MOI) in the presence or absence of 5 μM OSC. A. The firmly adherent neutrophils were counted after the H37Rv infection for 6, 12, 18, and 24 h. B. F-actin polymerization was monitored using immunofluorescent microscopy at 24 h after the H37Rv infection. C. A Western blot analysis was performed to assess the expressions of TLR2, MyD88, Src, p-ERK1/2, ERK1/2, p-p38 MAPK, p38 MAPK, p-JNK, and JNK at 24 h after the H37Rv infection. β-actin was used as an endogenous control. D and E. The neutrophils were preincubated with the Src kinase inhibitor PP1 (5 μM), ERK1/2 inhibitor U0126 (10 μM), p38MAPK inhibitor SB202190 (10 μM), or the JNK inhibitor AG490 (25 μM) for 30 min or pretransfected with siTLR2 (100 nM) for 24 h, and then uninfected or infected with H37Rv (5 MOI) in the presence or absence of OSC (5 μM) for 24 h. D. The firmly adherent neutrophils were counted. E. F-actin polymerization was monitored. Data are expressed as the mean ± SD of the three independent experiments. *P < 0.05, **P < 0.01 compared with Ctrl group. #P < 0.05 compared with the Mtb group. Ctrl: control; OSC: Oxysophocarpine; NS: no significance.

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Oxysophocarpine reduces oxidative stress and inflammation in tuberculosis-infected neutrophils and mouse lungs

doi:

Figure Lengend Snippet: OSC hindered the adhesion and F-actin polymerization in the H37Rv-infected neutrophils by the inhibition of the TLR2/MyD88/Src/ERK1/2 signaling pathway. A-C. The neutrophils were uninfected or infected with H37Rv (5 MOI) in the presence or absence of 5 μM OSC. A. The firmly adherent neutrophils were counted after the H37Rv infection for 6, 12, 18, and 24 h. B. F-actin polymerization was monitored using immunofluorescent microscopy at 24 h after the H37Rv infection. C. A Western blot analysis was performed to assess the expressions of TLR2, MyD88, Src, p-ERK1/2, ERK1/2, p-p38 MAPK, p38 MAPK, p-JNK, and JNK at 24 h after the H37Rv infection. β-actin was used as an endogenous control. D and E. The neutrophils were preincubated with the Src kinase inhibitor PP1 (5 μM), ERK1/2 inhibitor U0126 (10 μM), p38MAPK inhibitor SB202190 (10 μM), or the JNK inhibitor AG490 (25 μM) for 30 min or pretransfected with siTLR2 (100 nM) for 24 h, and then uninfected or infected with H37Rv (5 MOI) in the presence or absence of OSC (5 μM) for 24 h. D. The firmly adherent neutrophils were counted. E. F-actin polymerization was monitored. Data are expressed as the mean ± SD of the three independent experiments. *P < 0.05, **P < 0.01 compared with Ctrl group. #P < 0.05 compared with the Mtb group. Ctrl: control; OSC: Oxysophocarpine; NS: no significance.

Article Snippet: Adhesion assay After pretreatment with the Src kinase inhibitor PP1 (5 μM), ERK1/2 inhibitor U0126 (10 μM), p38MAPK inhibitor SB202190 (10 μM), or JNK inhibitor AG490 (25 μM; Biomol, Plymouth Meeting, PA, USA) for 30 min or with siRNA targeting TLR2 (siTLR2; 100 nM; Santa Cruz Biotechnology, Inc., Dallas, Texas, USA) for 24 h, neutrophils (3 × 10 5 cells/well) were then uninfected or infected with H37Rv (5 MOI) in the presence or absence of 5 μM OSC and allowed to adhere to 48-well plates for 6, 12, 18, and 24 h. The non-adherent cells were washed away, and the adherent neutrophils were quantified using a myeloperoxidase (MPO) assay.

Techniques: Infection, Inhibition, Microscopy, Western Blot, Control