Resveratrol alleviates endometriosis via restoration of hypoxic milieu and inhibition of autoantibody deposition

Yi Luo, Luo Y, Mio Kobayashi, Kobayashi M, Di Zhang, Zhang D, Ono Y, Yosuke Ono, Osamu Yoshino, Yoshino O, Kanehira M, Masahiko Kanehira
Experimental animals · 2026 · doi:10.1538/expanim.26-0002 · PMID:42108087
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Resveratrol reduced endometriotic lesion size in mice by decreasing peritoneal hypoxia and inhibiting autoantibody deposition, proposing a new disease mechanism and therapeutic strategy.

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The paper studied whether resveratrol affects a proposed mechanism of endometriosis in a murine endometriosis model, using peritoneal hypoxia and innate immune activation as readouts. The authors induced a marked hypoxic state in the peritoneal cavity, showing increased HIF-1α expression in peritoneal exudate cells and upregulation of TLR4 and IL-1β, and then tested resveratrol as a hypoxia-reducing agent; resveratrol reduced HIF-1α–positive cells and significantly decreased the size and weight of endometriotic lesions. A key caveat noted in the results was that resveratrol did not alter TLR4 and IL-1β expression levels. The authors also reported that autoantibody deposition accumulated in endometriotic lesions and was inhibited by resveratrol, proposing autoantibody deposition as another causal concept. This paper is centrally about endometriosis — it examines resveratrol’s ability to reduce lesion burden by restoring a hypoxic milieu and inhibiting autoantibody deposition.

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Abstract

Endometriosis, a chronic disease that affects about 10% of women of reproductive age, is characterized by severe pain and growth of endometrium-like tissues outside the uteri. Although several theories have been advanced for the cause of endometriosis, no theory fully explains why endometriosis occurs. For this study, we strove to elucidate a new mechanism of endometriosis leading to establishment of a new therapeutic strategy for its treatment. In our murine endometriosis model, a marked hypoxic state was induced in the peritoneal cavity, as indicated by increased expression of HIF-1α in peritoneal exudate cells. Moreover, innate immune response, such as TLR4 and IL-1β expression, was upregulated. To restore the hypoxic milieu in endometriosis, we chose resveratrol (RSV), a natural polyphenolic compound, as a hypoxia-reducing agent. As expected, RSV administration decreased the number of HIF-1α-positive cells. Furthermore, RSV administration reduced the size and weight of endometriotic lesions significantly. However, RSV administration did not change TLR4 and IL-1β expression levels in peritoneal exudate cells. In the process of seeking mechanisms of endometriosis other than TLR4-dependent and IL-1β-dependent pathways, we detected autoantibody deposition in endometriotic lesions. In endometriotic lesions from RSV-administered mice, accumulation of autoantibodies was inhibited compared to a control group. As described herein, we proposed a new concept by which autoantibody deposition can cause endometriosis, raising the possibility of RSV as a promising therapeutic option for endometriosis.
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Resveratrol alleviates endometriosis via restoration of hypoxic milieu and inhibition of autoantibody deposition Article ID: 26-0002 Details Abstract Endometriosis, a chronic disease that affects about 10% of women of reproductive age, is characterized by severe pain and growth of endometrium-like tissues outside the uteri. Although several theories have been advanced for the cause of endometriosis, no theory fully explains why endometriosis occurs. For this study, we strove to elucidate a new mechanism of endometriosis leading to establishment of a new therapeutic strategy for its treatment. In our murine endometriosis model, a marked hypoxic state was induced in the peritoneal cavity, as indicated by increased expression of HIF-1α in peritoneal exudate cells. Moreover, innate immune response, such as TLR4 and IL-1β expression, was upregulated. To restore the hypoxic milieu in endometriosis, we chose resveratrol (RSV), a natural polyphenolic compound, as a hypoxia-reducing agent. As expected, RSV administration decreased the number of HIF-1α–positive cells. Furthermore, RSV administration reduced the size and weight of endometriotic lesions significantly. However, RSV administration did not change TLR4 and IL-1β expression levels in peritoneal exudate cells. In the process of seeking mechanisms of endometriosis other than TLR4-dependent and IL-1β-dependent pathways, we detected autoantibody deposition in endometriotic lesions. In endometriotic lesions from RSV-administered mice, accumulation of autoantibodies was inhibited compared to a control group. As described herein, we proposed a new concept by which autoantibody deposition can cause endometriosis, raising the possibility of RSV as a promising therapeutic option for endometriosis. © 2026 Japanese Association for Laboratory Animal Science This article is licensed under a Creative Commons [Attribution-NonCommercial-NoDerivatives 4.0 International] license. https://creativecommons.org/licenses/by-nc-nd/4.0/ Favorites & Alerts Recently viewed articles

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endometriosis

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chemicals 2
resveratrol resveratrol
organisms 5
tenuivirus oryzaclavatae tenuivirus oryzaclavatae tenuivirus oryzaclavatae mus sp. tenuivirus oryzaclavatae

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