Jin-Ya Wang1, Xiaoyan Dong2, Zhiwei Yu3, Lei Ge4, Lu Lu4, Ling Ding4, Weihua Gan5. 1. Department of Pediatrics, The Second Affiliated Hospital of Nanjing Medical University, 262 Zhongshan North Road, Nanjing, Jiangsu 210003, China. Electronic address: jinyawang@vip.163.com. 2. Department of Pulmonary, Shanghai Children's Hospital, Shanghai Jiaotong University Shanghai, China. 3. Department of Pediatrics, The Second Affiliated Hospital of Nanjing Medical University, 262 Zhongshan North Road, Nanjing, Jiangsu 210003, China; Department of Pediatrics, The Affiliated Wuxi Children's Hospital of Nanjing Medical University, Wuxi 214023, Jiangsu, China. 4. Department of Pediatrics, The Second Affiliated Hospital of Nanjing Medical University, 262 Zhongshan North Road, Nanjing, Jiangsu 210003, China. 5. Department of Pediatrics, The Second Affiliated Hospital of Nanjing Medical University, 262 Zhongshan North Road, Nanjing, Jiangsu 210003, China. Electronic address: article1886@njmu.edu.cn.
Abstract
BACKGROUND: Asthma is a chronic airway inflammatory disease caused by a variety of cytokines and signaling pathways closely related to immunoregulation. Corticosteroids are the most widely used drug in the asthma treatment. However, the use of corticosteroids could cause topical side effects. So, it's important to find new drugs for asthma treatment. Our study aims to explore the pharmacological effect of borneol on asthma and its underlying mechanism. METHODS: We constructed the OVA-induced asthma model to investigate the effect of borneol on asthma in mice. HE and PAS staining was used to detect the effect of borneol on pathological change of mice with asthma. Inflammatory cytokines were measured by ELISA. qRT-PCR was used to explore the effect of borneol on microRNAs expression. Cell proliferation of CD4 + T cells was detected by CCK-8 assay and flow cytometry. Western blot was used to detect pten expression and Akt activation. RESULTS: We found that borneol significantly alleviated asthma progression in mice. Borneol inhibited CD4 + T cells infiltration in vivo and proliferation in vitro by downregulating miR-26a and miR-142-3p. miR-26a and miR-142-3p promoted CD4 + T cells proliferation in vitro through targeting Pten. Overexpression of miR-26a and miR-142-3p abolished the effect of borneol in vivo. CONCLUSION: In a word, these findings suggested that borneol attenuated asthma in mice by decreasing the CD4 + T cells infiltration. The molecular mechanism of borneol was dependent on the downregulation of miR-26a and miR-142-3p to upregulate the Pten expression.
BACKGROUND:Asthma is a chronic airway inflammatory disease caused by a variety of cytokines and signaling pathways closely related to immunoregulation. Corticosteroids are the most widely used drug in the asthma treatment. However, the use of corticosteroids could cause topical side effects. So, it's important to find new drugs for asthma treatment. Our study aims to explore the pharmacological effect of borneol on asthma and its underlying mechanism. METHODS: We constructed the OVA-induced asthma model to investigate the effect of borneol on asthma in mice. HE and PAS staining was used to detect the effect of borneol on pathological change of mice with asthma. Inflammatory cytokines were measured by ELISA. qRT-PCR was used to explore the effect of borneol on microRNAs expression. Cell proliferation of CD4 + T cells was detected by CCK-8 assay and flow cytometry. Western blot was used to detect pten expression and Akt activation. RESULTS: We found that borneol significantly alleviated asthma progression in mice. Borneol inhibited CD4 + T cells infiltration in vivo and proliferation in vitro by downregulating miR-26a and miR-142-3p. miR-26a and miR-142-3p promoted CD4 + T cells proliferation in vitro through targeting Pten. Overexpression of miR-26a and miR-142-3p abolished the effect of borneol in vivo. CONCLUSION: In a word, these findings suggested that borneol attenuated asthma in mice by decreasing the CD4 + T cells infiltration. The molecular mechanism of borneol was dependent on the downregulation of miR-26a and miR-142-3p to upregulate the Pten expression.
Authors: Nadghia F Leite-Sampaio; Cicera N F L Gondim; Rachel A A Martins; Abolghasem Siyadatpanah; Roghayeh Norouzi; Bonglee Kim; Celestina E Sobral-Souza; Gonçalo E C Gondim; Jaime Ribeiro-Filho; Henrique D M Coutinho Journal: Biomed Res Int Date: 2022-05-25 Impact factor: 3.246
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