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Background <p>Aflatoxin B<sub>1</sub> (AFB<sub>1</sub>) risks animal and human health, and the liver is considered the most crucial detoxification organ. Phlorotannin (PT) is a polyhydroxy phenol that has a wide range of biological activities, including anti-oxidation and hepatoprotection, which can promote the ability of liver detoxification. This study aimed to elucidate the protective effect of PT on AFB<sub>1</sub>-induced liver damage in broilers.</p> Results <p>In vivo experiment showed that the PT reduced AFB<sub>1</sub> content and AFB<sub>1</sub>-exo-8,9-epoxide DNA (AFBO-DNA) concentration in serum and liver (<i>P</i> &lt; 0.05), improved the histomorphology of liver and hepatic mitochondria, and activated nuclear factor erythroid 2-related factor 2 (Nrf2)-related antioxidant and detoxification pathway by upregulating the activities of antioxidant enzymes (catalase [CAT], glutathione S-transferase [GST]) and total antioxidant capacity (T-AOC) level&#xa0;(<i>P</i> &lt; 0.05), and inhibited the mRNA expression of <i>CYP1A1 </i>(cytochrome P450 family 1 subfamily A member 1) and phase II detoxification enzyme related genes (<i>GPX1</i>, <i>GSTT1</i>, and&#xa0;<i>NQO1</i>) of broilers exposed to AFB<sub>1&#xa0;</sub>(<i>P</i> &lt; 0.05). Meanwhile, PT upregulated the Nrf1 pathway-related mitochondrial biosynthetic genes (<i>Nrf1</i>, mitochondrial transcription factor A [<i>TFAM</i>], mitofusin 1 [<i>MFN1</i>]) in broilers fed AFB<sub>1</sub> contaminated diet&#xa0;(<i>P</i> &lt; 0.05). In vitro verification study suggested that the use of Nrf2/Nrf1 inhibitors suppressed the ameliorative role of PT on AFB<sub>1</sub>-induced liver injury of broilers, which was manifested in the mRNA expression of <i>Nrf2</i>, <i>NQO1</i>, <i>GSTT3</i>, <i>Nrf1</i>, <i>TFAM</i>, and other genes decreasing (<i>P</i> &lt; 0.05), and down-regulation of the protein expression of Nrf2, total and nucleus p-Nrf2, and total and nucleus p-Nrf1 (<i>P</i> &lt; 0.05).</p> Conclusion <p>The PT ameliorates oxidative stress and hepatotoxicity by activating the Nrf2-mediated phase II detoxification enzymes pathway and maintains mitochondrial homeostasis by activating the Nrf1 signaling pathway in broilers exposed to AFB<sub>1</sub>.</p> Graphical Abstract <p></p>

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The ameliorative role of phlorotannin on aflatoxin B1-induced liver oxidative stress and mitochondrial injury is related to the activation of Nrf2 and Nrf1 signaling pathways in broilers

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月22日

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  • Xueqing Ye,
  • Yuying Yang,
  • Qinghua Yao,
  • Mengyi Huang,
  • Balamuralikrishnan Balasubramanian,
  • Rajesh Jha,
  • Wenchao Liu

摘要

Background

Aflatoxin B1 (AFB1) risks animal and human health, and the liver is considered the most crucial detoxification organ. Phlorotannin (PT) is a polyhydroxy phenol that has a wide range of biological activities, including anti-oxidation and hepatoprotection, which can promote the ability of liver detoxification. This study aimed to elucidate the protective effect of PT on AFB1-induced liver damage in broilers.

Results

In vivo experiment showed that the PT reduced AFB1 content and AFB1-exo-8,9-epoxide DNA (AFBO-DNA) concentration in serum and liver (P < 0.05), improved the histomorphology of liver and hepatic mitochondria, and activated nuclear factor erythroid 2-related factor 2 (Nrf2)-related antioxidant and detoxification pathway by upregulating the activities of antioxidant enzymes (catalase [CAT], glutathione S-transferase [GST]) and total antioxidant capacity (T-AOC) level (P < 0.05), and inhibited the mRNA expression of CYP1A1 (cytochrome P450 family 1 subfamily A member 1) and phase II detoxification enzyme related genes (GPX1, GSTT1, and NQO1) of broilers exposed to AFB1 (P < 0.05). Meanwhile, PT upregulated the Nrf1 pathway-related mitochondrial biosynthetic genes (Nrf1, mitochondrial transcription factor A [TFAM], mitofusin 1 [MFN1]) in broilers fed AFB1 contaminated diet (P < 0.05). In vitro verification study suggested that the use of Nrf2/Nrf1 inhibitors suppressed the ameliorative role of PT on AFB1-induced liver injury of broilers, which was manifested in the mRNA expression of Nrf2, NQO1, GSTT3, Nrf1, TFAM, and other genes decreasing (P < 0.05), and down-regulation of the protein expression of Nrf2, total and nucleus p-Nrf2, and total and nucleus p-Nrf1 (P < 0.05).

Conclusion

The PT ameliorates oxidative stress and hepatotoxicity by activating the Nrf2-mediated phase II detoxification enzymes pathway and maintains mitochondrial homeostasis by activating the Nrf1 signaling pathway in broilers exposed to AFB1.

Graphical Abstract