Fig 1: Effects of BDNF@Hb-PDA@DEX@gel treatment on neurogenesis after TBI. (A) Representative images of NeuN+ (green fluorescence), BrdU+ (red fluorescence), SOX2+ (red fluorescence) and DCX+ (red fluorescence) cells in hippocampal DG area (Scale bar: 100 µm) ; (B) Quantification of BrdU+/NeuN+ cells on post-injury day 21 [one-way ANOVA, F (4, 25) = 59, P < 0.0001, η²=0.9]; (C) Quantification of SOX2 + cells on post-injury day 3 and 21 [one-way ANOVA, F (4, 25) = 327.4, P < 0.0001, η²=0.98 for post-injury day 3; F (4, 25) = 307.8, P < 0.0001, η²=0.98 for post-injury day 21]; (D) Quantification of DCX+ cells on post-injury day 3 and 21 [one-way ANOVA, F (4, 25) = 59.35, P < 0.0001, η²=0.9 for post-injury day 3; F (4, 25) = 423.7, P < 0.0001, η²=0.99 for post-injury day 21]. *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001. The data are presented as the means ± SD (n = 6)
Fig 2: BDNF@Hb-PDA@DEX@gel treatment inhibits neuroinflammation after TBI. (A, B) Representative images of Iba+ (red fluorescence) and CD16/32 + cells (green fluorescence) (Scale bar: 50 µm); (C-F) Quantification of Iba+, and Iba+/CD16/32 + cells in ipsilateral cortex and hippocampus on post-injury day 3 [one-way ANOVA, F (4, 25) = 302.4, P < 0.0001, η²=0.98 for cortex; F (4, 25) = 331.1, P < 0.0001, η²=0.98 for hippocampus]; (G-I) Quantification of IL-1β, IL-6, and TNF-α levels in the ipsilateral hemisphere [one-way ANOVA, F (4, 25) = 72.2, P < 0.0001, η²=0.92 for IL-1β; F (4, 25) = 93.32, P < 0.0001, η²=0.94 for IL-6; F (4, 25) = 52.53, P < 0.0001, η²=0.89 for TNF-α ]. *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001. The data are presented as the means ± SD (n = 6)
Fig 3: Effects of BDNF@Hb-PDA@DEX@gel treatment on angiogenesis after TBI. (A) Representative images of CD31 + cells in the ipsilateral cortex and hippocampus (red fluorescence) (Scale bar: 50 µm); (B-E) Quantification of CD31 + cells in the ipsilateral cortex and hippocampus on post-injury day 3 and 21 [one-way ANOVA, F (4, 25) = 74.19, P < 0.0001, η²=0.92 for cortex on post-injury day 3; F (4, 25) = 48.06, P < 0.0001, η²=0.88 for hippocampus on post-injury day 3; F (4, 25) = 47.87, P < 0.0001, η²=0.88 for cortex on post-injury day 21; F (4, 25) = 45.58, P < 0.0001, η²=0.87 for hippocampus on post-injury day 21]. *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001. The data are presented as the means ± SD (n = 6)
Fig 4: Preparation and characteristics of BDNF@Hb-PDA@DEX NPs. (A-C) TEM images of Hb, BDNF@Hb, and BDNF@Hb-PDA@DEX (Scale bar: 100 nm); (D, E) DLS size distribution of BDNF@Hb, and BDNF@Hb-PDA@DEX; (F) Size stability of BDNF@Hb and BDNF@Hb-PDA@DEX; (G) Zeta potential of Hb, BDNF@Hb, BDNF@Hb-PDA, and BDNF@Hb-PDA@DEX; (H) FTIR spectra of BDNF@Hb and BDNF@Hb-PDA@DEX; (I) TGA analysis of BDNF@Hb and BDNF@Hb-PDA@DEX. Data are presented as means ± SD (n = 3)
Fig 5: Schematic illustration showing the synthesis, intraoperative local administration and multifunctional roles of BDNF@Hb-PDA@DEX@gel in TBI. (A) Illustration of the synthesis and characteristics of BDNF@Hb-PDA@DEX@gel; (B) Intraoperative local administration of BDNF@Hb-PDA@DEX@gel after CCI. BDNF@Hb-PDA@DEX@gel can effectively reduce the acute-phase inflammatory response, protect the blood - brain barrier, alleviate cerebral edema, and may promote angiogenesis, and proliferation and differentiation of neural stem cells in the late inflammatory stage after CCI
Supplier Page from Abcam for Recombinant Human BDNF protein