Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway Cell Physiol Biochem 2017;43:481–491 - DOI:10.1159/000480474.

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Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway Cell Physiol Biochem 2017;43:481–491 - DOI:10.1159/000480474 Fig. 1. Basso, Beattie and Bresnahan (BBB) scores of rats in each group at different time points after injury. The BBB scores were evaluated at 24, 48, 72 hours after sham surgery or spinal cord injury, n =8/group for all the groups. Results are expressed as the mean±S.D. from three independent experiments.** P<0.01 versus SCI group, *** P<0.001 versus SCI group. © 2017 The Author(s). Published by S. Karger AG, Basel - CC BY-NC-ND 4.0

Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway Cell Physiol Biochem 2017;43:481–491 - DOI:10.1159/000480474 Fig. 2. Effects of shikonin on the tissue repair in the spinal cord in rats with spinal cord injury. The spinal cord tissue harvested at 72 h after injury was subject to HE staining. The results presented are representative. © 2017 The Author(s). Published by S. Karger AG, Basel - CC BY-NC-ND 4.0

Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway Cell Physiol Biochem 2017;43:481–491 - DOI:10.1159/000480474 Fig. 3. SHI diminishes the water content and inhibits the inflammation levels after SCI. (a) SHI treatment significantly attenuated SCI-induced spinal corded ema in rats. Quantification data of IL-1β (b), IL-6 (c), TNF-α (d) production in the spinal cord at 72 h after injury, as assessed by ELISA. Results are expressed as the mean±S.D. from three independent experiments. ** P<0.01 versus SCI group. © 2017 The Author(s). Published by S. Karger AG, Basel - CC BY-NC-ND 4.0

Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway Cell Physiol Biochem 2017;43:481–491 - DOI:10.1159/000480474 Fig. 4. Expression of HMGB1, TLR4, NF-κB after SCI injury in each group. (a) The protein levels of HMGB1, TLR4, NF-κB at 72 h post injury. The mRNA expression of HMGB1(a), TLR4 (b), NF-κB (c) and at 72 h post injury. Results are expressed as the mean±S.D. from three independent experiments. * P<0.05 versus SCI group, ** P<0.01 versus SCI group. © 2017 The Author(s). Published by S. Karger AG, Basel - CC BY-NC-ND 4.0

Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway Cell Physiol Biochem 2017;43:481–491 - DOI:10.1159/000480474 Fig. 5. Shikonin regulated inflammation through HMGB1 signaling. (a) The protein levels of HMGB1, TLR4, NF-κB at 72 h post injury. Quantification data of IL-1β (b), IL-6 (c), TNF-α (d) production in the spinal cord at 72 h after injury, as assessed by ELISA. Results are expressed as the mean±S.D. from three independent experiments. * P<0.05 versus MPSS group, ** P<0.01 versus SHI group. © 2017 The Author(s). Published by S. Karger AG, Basel - CC BY-NC-ND 4.0

Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway Cell Physiol Biochem 2017;43:481–491 - DOI:10.1159/000480474 Fig. 6. Effect of shikonin on apoptosis in spinal cord tissue of rats with spinal cordinjury. (a) Apoptotic cells in spinal cord tissue of rats (TUNEL staining, × 200), (b) Quantification of apoptotic cells in spinal cord tissue. (c) Shikonin inhibit caspase-3 protein expression. Results are expressed as the mean±S.D. from three independent experiments. ** P<0.01 versus SCI group， *** P<0.001 versus SCI group. © 2017 The Author(s). Published by S. Karger AG, Basel - CC BY-NC-ND 4.0

Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway Cell Physiol Biochem 2017;43:481–491 - DOI:10.1159/000480474 Fig. 7. Effect of shikonin on tissue repair in the spinal cord. (a) Representative photomicrographs of the spinal cord sections of mice subjected to each treatment showing IBA-1 immunoreactive cells at 72 hours after injury. (b) GFAP immunoreactivity to the injury site at 72 hours post-injury. © 2017 The Author(s). Published by S. Karger AG, Basel - CC BY-NC-ND 4.0