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. 1998 Feb 17;95(4):1894–1898. doi: 10.1073/pnas.95.4.1894

Figure 4.

Figure 4

The protective effects of [Nle59]hIGF-I and the IGFBP ligand inhibitor on ischemic brain damage. (A) In the first series of experiments, the effect of concurrent administration of [Nle59]hIGF-I or [Leu24,59,60, Ala31]hIGF-I was determined. Data are presented as mean lesion volume ± SEM. Animals injected at the time of MCAo with [Nle59]hIGF-I (50 μg, n = 7, open bar) or the IGFBP ligand inhibitor, [Leu24,59,60, Ala31]hIGF-I (50 μg, n = 6, gray bar) had dramatically and statistically reduced lesion volumes compared with animals injected with vehicle (n = 6, solid bar). Protection was observed in cerebral cortical and striatal tissue. ∗∗∗, P < 0.001. (B) The effects of delaying administration of [Nle59]hIGF-I or the IGFBP ligand inhibitor [Leu24,59,60, Ala31]hIGF-I were determined in a separate series of experiments. Data are presented as the percentage of the mean lesion size of the respective vehicle-treated group (mean ± SEM). As observed in the previous experiment, animals injected at the time of MCAo with [Nle59]hIGF-I (50 μg, n = 7, striped bar) or the IGFBP ligand inhibitor (50 μg, n = 6, striped bar) had dramatically and statistically reduced lesion volumes compared with animals injected with vehicle (n = 6, solid bar). When administration of the peptide was delayed to 1 h after MCAo, protection with [Nle59]hIGF-I (50 μg, n = 7, gray bar) was remarkably similar, and protection with IGFBP ligand inhibitor (50 μg, n = 8, gray bar) was only slightly less than observed with concurrent administration. ∗∗, P < 0.01; ∗∗∗, P < 0.001.