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Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Semaphone 3A (Sema3A) is an important neurovascular growth inhibitor. It is not clear how Sema3A is involved in the pathogenesis of discogenic low back pain. Exploring the potential mechanism of Sema3A in intervertebral disc degeneration can provide a new target and theoretical basis for the prevention and treatment of discogenic low back pain. OBJECTIVE: To explore the mechanism of interleukin-1β inhibiting the expression of Sema3A by activating the nuclear factor-κB signaling pathway to induce intervertebral disc degeneration in rats. METHODS: RT-qPCR was used to detect the expression of Sema3A mRNA in normal and degenerative human nucleus pulposus tissues. Nucleus pulposus cells of Sprague-Dawley rats were isolated, cultured, and passaged to the 3rd generation. Then, passage 3 cells were divided into three groups: the blank control group was routinely cultured for 48 hours, the degeneration group was intervened with 10 ng/mL interleukin 1β for 48 hours, and the degeneration+inhibitor group was treated by 5 µmol/L nuclear factor-κB signaling pathway-specific inhibitor BAY11-7082 for 1 hour, followed by interleukin-1β for 48 hours. At the end of the intervention, cell viability was detected by cell counting kit-8, cell apoptosis was detected by Annexin V/FITC staining, mRNA expression of cellular matrix, vascular and neural markers and Sema3A was detected by RT-qPCR, and protein expression of marker proteins, p65 and p-p65 was detected by western blot. RESULTS AND CONCLUSION: RT-qPCR assay showed that the expression of Sema3A mRNA was lower in degenerative human nucleus pulposus tissue than in normal human nucleus pulposus tissue (P < 0.05). Compared with the blank control group, the nucleus pulposus cell viability decreased and the apoptotic rate increased in the degeneration group (P < 0.05); compared with the degeneration group, the nucleus pulposus cell viability increased and the apoptotic rate decreased in the degeneration + inhibitor group (P < 0.05). Compared with the blank control group, mRNA expression of type II collagen, polyproteoglycan, and Sema3A was decreased in the degeneration group (P < 0.05), while mRNA expression of CD31 and neurofilament 200 was increased (P < 0.05). Compared with the degeneration group, mRNA expression of type II collagen, polyproteoglycan, and Sema3A was elevated in the degeneration+inhibitor group (P < 0.05) and mRNA expression of CD31 and neurofilament 200 decreased (P < 0.05). Compared with the blank control group, the protein expression of type II collagen, polyproteoglycan, and Sema3A was decreased in the degeneration group (P < 0.05), and the protein expression of CD31, neurofilament protein 200, p65, and p-p65 was elevated (P < 0.05); compared with the degeneration group, the protein expression of type II collagen, polyproteoglycan, and Sema3A was elevated in the degeneration+inhibitor group (P < 0.05), and protein expression of CD31, neurofilament 200, p65, and p-p65 was decreased (P < 0.05). To conclude, interleukin-1β does inhibit the expression of Sema3A by activating the nuclear factor-κB signaling pathway, which can also increase the degradation of extracellular matrix, promote the innervation and angiogenesis in degenerative intervertebral disc, and may be one of potential factors that contribute to intervertebral disc degeneration and discogenic low back pain. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Previous studies showed that immunomodulatory peptide DP7 has good antibacterial activity and immunomodulatory activity in vitro. OBJECTIVE: To investigate the therapeutic effect of a new type of immunoregulatory peptide DP7 temperature-sensitive gel on periodontitis in rats. METHODS: The periodontitis model of right maxillary first molar was established in 8-week-old SD rats, and the 48 successfully modeled rats were divided into 6 groups. Except for the natural healing group without treatment, minocycline hydrochloride was injected into periodontal pocket of positive control group. The periodontal pocket of the rest of the four groups were injected with regulatory peptide DP7 concentration 0%（blank gel）, 0.1%, 0.3%, 1% temperature sensitive gel, once a week for 4 weeks. Four weeks later, the periodontal probing depth and the distance between cementum enamel boundary and alveolar crest were examined; and histological and immunohistochemical staining of the right maxilla was performed. RESULTS AND CONCLUSION: (1) The probing depth and the distance between cementum enamel boundary and alveolar crest in 1% and 0.3% DP7 gel treatment groups were lower than those in positive control group (P < 0.05). (2) Hematoxylin-eosin staining showed that the gingival tissue of 0.1%, 0.3%, 1% DP7 gel groups and positive control group was more complete, and the epithelial pedicle process returned to normal, with the orderly array of fibroblasts and new capillaries, and no obvious osteoclasts were observed. The blank gel treatment group and the natural healing group showed the pathological manifestations of periodontitis. (3) Masson staining showed that a large number of new fibroblasts were orderly arranged in the 0.1%, 0.3%, and 1% DP7 gel groups and the positive control group, and bulging collagen hyperplasia and new capillaries were visible. Osteoid or new bone formation was even observed in the 1% and 0.3% DP7 gel groups. However, the blank gel group and the natural healing group had no obvious collagen fiber proliferation and osteoid formation. (4) Immunohistochemical staining showed that the expression levels of tumor necrosis factor-α and interleukin-1β in 0.3% and 1% DP7 gel groups were not significantly different from those in the positive control group (P > 0.05). The expression levels of interleukin-10, bone morphogenetic protein-2 and osteoblast specific transcription factor 2 in 0.3% and 1% DP7 gel groups were higher than those in the positive control group (P=0.000). The expression levels of interleukin-10, bone morphogenetic protein-2 and osteoblast specific transcription factor 2 in 0.3% DP7 gel group were higher than those in the 1% DP7 gel group (P < 0.05). (5) The results showed that 0.3% and 1% immunoregulatory peptide DP7 gel had favorable therapeutic effect on periodontitis, and 0.3% immunoregulatory peptide DP7 gel had the best therapeutic effect. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)