Baicalin alleviates endometrial inflammatory injury through regulation of tight junction proteins

Yang, Diqi; Yin, Ruiling; Lei, Qianghui; Zhu, Jiandi; Nan, Sha; Ma, Ning; Zhu, Hongmei; Chen, Jianguo; Han, Li; Ding, Mingxing; Ding, Yi

doi:10.1039/d2fo00594h

Cited by 7 publications

(1 citation statement)

References 38 publications

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“…In a mycobacterium tuberculosis‐infected model, BA acts as an anti‐inflammatory agent by means of inducing autophagy (Zhang et al, 2017). BA regulated autophagy and then redistribution of TJ proteins against inflammatory injury (Yang, Yin, et al, 2022). BA can also alleviate Mycoplasma oxidative stress and apoptosis by regulating the NLRP3‐autophagy pathway (Byun et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Baicalin promotes random‐pattern skin flap survival by inducing autophagy via AMPK‐regulated TFEB nuclear transcription

Zhang

et al. 2023

Phytotherapy Research

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The random‐pattern skin flap is a generally used technique to cover the soft tissue defect, while its application is often constrained by complications after the flap transplant. Necrosis of the flap remains a principal obstacle. The purpose of this study was to investigate the effect of Baicalin on skin flap survival and its mechanism. First of all, we discovered that administering Baicalin stimulated cell migration and boosted the formation of capillary tubes in human umbilical vein endothelial cells. Then, we detected that Baicalin reduced apoptosis‐induced oxidative stress by using western blot and oxidative stress test kit. After that, we observed that Baicalin increased autophagy and utilized 3MA to block autophagy augmentation substantially reversing the effects of Baicalin therapy. Furthermore, we uncovered the underlying mechanisms of Baicalin‐induced autophagy via AMPK‐regulated TFEB nuclear transcription. Finally, our in vivo experiment findings showed that Baicalin reduces oxidative stress, inhibits apoptosis, promotes angiogenesis, and boosts the levels of autophagy. After autophagy was blocked, substantially reversing the effects of Baicalin therapy. Our study indicated that Baicalin‐induced autophagy via AMPK regulated TFEB nuclear transcription and then promotes angiogenesis and against oxidative stress and apoptotic promotes skin flap survival. These findings highlight the therapeutic potential for the clinical application of Baicalin in the future.

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Section: Discussionmentioning

confidence: 99%

Baicalin promotes random‐pattern skin flap survival by inducing autophagy via AMPK‐regulated TFEB nuclear transcription

Zhang

et al. 2023

Phytotherapy Research

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Baicalin methyl ester prevents the LPS – induced mice intestinal barrier damage in vivo and in vitro via P65/TNF-α/MLCK/ZO-1 signal pathway

Liang,

Sun,

Guo

et al. 2024

Biomedicine & Pharmacotherapy

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Arachidonic acid impairs the function of the blood-testis barrier via triggering mitochondrial complex-ROS-P38 MAPK axis in hyperthermal Sertoli cells

Huang

et al. 2023

Ecotoxicology and Environmental Safety

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Baicalin alleviates endometrial inflammatory injury through regulation of tight junction proteins

Abstract: Baicalin alleviates endometrial inflammatory injury in a mouse model. Baicalin activated autophagy in a mouse model and a cell model. Baicalin redistributed TJ proteins by regulating autophagy.

Cited by 7 publications

References 38 publications

Baicalin promotes random‐pattern skin flap survival by inducing autophagy via AMPK‐regulated TFEB nuclear transcription

Baicalin promotes random‐pattern skin flap survival by inducing autophagy via AMPK‐regulated TFEB nuclear transcription

Baicalin methyl ester prevents the LPS – induced mice intestinal barrier damage in vivo and in vitro via P65/TNF-α/MLCK/ZO-1 signal pathway

Arachidonic acid impairs the function of the blood-testis barrier via triggering mitochondrial complex-ROS-P38 MAPK axis in hyperthermal Sertoli cells

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