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Betulinic Acid–Mediated NR1D1 Alleviates Dextran Sulfate Sodium–Induced Colitis in Mice by Modulating VDAC1/NF‐κВ.

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Title: Betulinic Acid–Mediated NR1D1 Alleviates Dextran Sulfate Sodium–Induced Colitis in Mice by Modulating VDAC1/NF‐κВ.
Authors: Zhang, Qikun1,2,3 (AUTHOR), Song, Ge4 (AUTHOR), Zhong, Rulei2,3 (AUTHOR), Wang, Haibo5 (AUTHOR), Liu, Zhiqiang1 (AUTHOR), Cui, Haodong1,2 (AUTHOR), Yin, Jimin1,2 (AUTHOR), Qi, Yong6 (AUTHOR) 15755188582@163.com, Wu, Wenyong1,2 (AUTHOR) wuwenyong@ahmu.edu.cn, Restivo, Ignazio (AUTHOR)
Source: Journal of Food Biochemistry. 6/13/2025, Vol. 2025, p1-17. 17p.
Subjects: Betulinic acid, Oral drug administration, Dextran sulfate, Colitis, Inflammatory bowel diseases, Laboratory mice
Abstract: Purpose: Inflammatory bowel disease (IBD) can severely disrupt intestinal health, leading to chronic inflammation. Betulinic acid (BHA) has demonstrated anti‐inflammatory and antioxidant properties. This study aims to explore the mechanism by which BHA alleviates colitis through the regulation of the key circadian gene REV‐ERBα (NR1D1) in a DSS‐induced colitis mouse model. Methods: The study first utilized in vivo experiments to establish a mouse model of colitis induced by DSS, investigating the effect of BHA in alleviating colitis through the regulation of NR1D1. Subsequently, an inflammatory model was established at the cellular level using CCD841 cells treated with 100 ng/mL LPS to explore the regulatory mechanism of BHA on colitis. Results: Our results indicate that oral administration of BHA effectively alleviates colitis symptoms, as shown by reduced disease activity index and histopathological scores. Notably, we found that BHA improves intestinal inflammation in DSS‐induced mice by downregulating VDAC1/NF‐κB. In addition, in vitro experiments demonstrate that the anti‐inflammatory effects of BHA are closely related to the NR1D1 gene. Conclusion: Our findings demonstrate the potential of BHA as a preventive and therapeutic agent for IBD. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Food Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. 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.)
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PubType: Academic Journal
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  Data: Betulinic Acid–Mediated NR1D1 Alleviates Dextran Sulfate Sodium–Induced Colitis in Mice by Modulating VDAC1/NF‐κВ.
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  Data: <searchLink fieldCode="AR" term="%22Zhang%2C+Qikun%22">Zhang, Qikun</searchLink><relatesTo>1,2,3</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Song%2C+Ge%22">Song, Ge</searchLink><relatesTo>4</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zhong%2C+Rulei%22">Zhong, Rulei</searchLink><relatesTo>2,3</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Wang%2C+Haibo%22">Wang, Haibo</searchLink><relatesTo>5</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Liu%2C+Zhiqiang%22">Liu, Zhiqiang</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Cui%2C+Haodong%22">Cui, Haodong</searchLink><relatesTo>1,2</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Yin%2C+Jimin%22">Yin, Jimin</searchLink><relatesTo>1,2</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Qi%2C+Yong%22">Qi, Yong</searchLink><relatesTo>6</relatesTo> (AUTHOR)<i> 15755188582@163.com</i><br /><searchLink fieldCode="AR" term="%22Wu%2C+Wenyong%22">Wu, Wenyong</searchLink><relatesTo>1,2</relatesTo> (AUTHOR)<i> wuwenyong@ahmu.edu.cn</i><br /><searchLink fieldCode="AR" term="%22Restivo%2C+Ignazio%22">Restivo, Ignazio</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22Journal+of+Food+Biochemistry%22">Journal of Food Biochemistry</searchLink>. 6/13/2025, Vol. 2025, p1-17. 17p.
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  Data: <searchLink fieldCode="DE" term="%22Betulinic+acid%22">Betulinic acid</searchLink><br /><searchLink fieldCode="DE" term="%22Oral+drug+administration%22">Oral drug administration</searchLink><br /><searchLink fieldCode="DE" term="%22Dextran+sulfate%22">Dextran sulfate</searchLink><br /><searchLink fieldCode="DE" term="%22Colitis%22">Colitis</searchLink><br /><searchLink fieldCode="DE" term="%22Inflammatory+bowel+diseases%22">Inflammatory bowel diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Laboratory+mice%22">Laboratory mice</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Purpose: Inflammatory bowel disease (IBD) can severely disrupt intestinal health, leading to chronic inflammation. Betulinic acid (BHA) has demonstrated anti‐inflammatory and antioxidant properties. This study aims to explore the mechanism by which BHA alleviates colitis through the regulation of the key circadian gene REV‐ERBα (NR1D1) in a DSS‐induced colitis mouse model. Methods: The study first utilized in vivo experiments to establish a mouse model of colitis induced by DSS, investigating the effect of BHA in alleviating colitis through the regulation of NR1D1. Subsequently, an inflammatory model was established at the cellular level using CCD841 cells treated with 100 ng/mL LPS to explore the regulatory mechanism of BHA on colitis. Results: Our results indicate that oral administration of BHA effectively alleviates colitis symptoms, as shown by reduced disease activity index and histopathological scores. Notably, we found that BHA improves intestinal inflammation in DSS‐induced mice by downregulating VDAC1/NF‐κB. In addition, in vitro experiments demonstrate that the anti‐inflammatory effects of BHA are closely related to the NR1D1 gene. Conclusion: Our findings demonstrate the potential of BHA as a preventive and therapeutic agent for IBD. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Journal of Food Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. 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.</i> (Copyright applies to all Abstracts.)
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      – Type: doi
        Value: 10.1155/jfbc/3244032
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      – Code: eng
        Text: English
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        PageCount: 17
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      – SubjectFull: Betulinic acid
        Type: general
      – SubjectFull: Oral drug administration
        Type: general
      – SubjectFull: Dextran sulfate
        Type: general
      – SubjectFull: Colitis
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      – SubjectFull: Inflammatory bowel diseases
        Type: general
      – SubjectFull: Laboratory mice
        Type: general
    Titles:
      – TitleFull: Betulinic Acid–Mediated NR1D1 Alleviates Dextran Sulfate Sodium–Induced Colitis in Mice by Modulating VDAC1/NF‐κВ.
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            – D: 13
              M: 06
              Text: 6/13/2025
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