Fig 1: Experimental design. The rats were intravenously injected with rt-PA for thrombolysis after 3 h of MCAO. Then the neurological deficits, TTC, infarct volumes, TEM assessments, cerebral hemorrhage, and the expressions of PKCδ, Marcks, and MMP-9 were conducted by IHC, WB, IF, or qRT-PCR at the indicated time points after thrombolysis. IF: immunofluorescence; IHC: immunohistochemistry; Marcks: myristoylated alanine-rich C-kinase substrate; MCAO: middle cerebral artery occlusion; MMP-9: matrix metalloproteinase 9; PKCδ: protein kinase C delta; qRT-PCR: quantitative real-time polymerase chain reaction; rt-PA, recombinant tissue plasminogen activator; TEM: transmission electronic microscope; TTC: 2,3,5-triphenyltetrazolium chloride; WB: Western blot.
Fig 2: Results of each group after each statistical analysis. The treatments with Ast + Lig, inhibitor rottlerin and Ast + Lig + rottlerin all reduced expression levels of PKCδ, Marcks, and MMP9. And the decrease in Ast + Lig + rottlerin group was the most significant (**P < 0.01, *P < 0.05, n = 6 in each group). Scale bar = 50 µm. Band intensities normalized to β-actin intensity. Ast: Astragalus membranaceus; Lig: ligustrazine; Marcks: myristoylated alanine-rich C-kinase substrate; MMP9: matrix metalloproteinase 9; PKCδ: protein kinase C delta.
Fig 3: The positive protein expression of PKCδ, Marcks, and MMP9 around the cerebral vessels in each group. Marcks: myristoylated alanine-rich C-kinase substrate; MMP9: matrix metalloproteinase 9; PKCδ: protein kinase C delta.
Supplier Page from Abcam for Anti-MARCKS antibody