Chengyi Miao
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Chengyi Miao has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Bian-Hua Zhou
College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan 471000, China
1 shared publication - Hong-Wei Wang
Henan Key Laboratory of Environmental and Animal Product Safety, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan 471000, China
1 shared publication - Jing Zhao
Henan Key Laboratory of Environmental and Animal Product Safety, Henan University of Science and Technology, Luoyang, People’s Republic of China
1 shared publication - Meng Gao
Henan Key Laboratory of Environmental and Animal Product Safety, Henan University of Science and Technology, Luoyang, People’s Republic of China
1 shared publication - Mohammad Mehdi Ommati
Henan Key Laboratory of Environmental and Animal Product Safety, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan 471000, China; Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz 71348-14336, Iran
1 shared publication - Sai Zhang
College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China
1 shared publication
Latest Publications
- 3 May 2025
- Published by Springer Nature in Biological Trace Element Research
- Vol. 203 (12) , 6192-6205
The NRF2/HO- 1 Pathway: a Potential Regulatory Factor in Fluoride-Induced Colonic Injury under Estrogen Deficiency
Our previous studies have demonstrated that fluoride (F) overexposure is a risk factor for colonic microenvironment, yet its underlying mechanisms and the influencing factors remain poorly understood. Here, a rat model of F exposure (0, 25, 50, 100 mg/L in drinking water) combined with ovariectomy (OVX)-induced estrogen deficiency was established to investigate the roles of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway in F-induced colonic damage under the state of estrogen deficiency. Result showed that F exposure significantly reduced occludin and claudin-1 expression, further resulting in the colon’s morphology impairment. Concurrently, F suppressed epithelial proliferation, decreased goblet cell numbers, and diminished short-chain fatty acid (SCFA) production. OVX-induced estrogen deficiency exacerbated F-induced colonic barrier damage and SCFA decreased. Mechanistically, estrogen deficiency aggravated F intestinal toxicity by further inhibiting the protein expression of Nrf2 and HO-1 and upregulating Keap1 protein expression, following downregulated Bcl-2 mRNA levels and upregulated Bax and caspase-3 mRNA levels, and promoting colonic epithelial cell apoptosis. These findings identify that Nrf2/HO-1 key protein disorders are involved in F-induced colonic barrier injury, and estrogen deficiency further aggravated F intestinal toxicity.
- 3 May 2025
- Published by Springer Nature in Biological Trace Element Research
- Vol. 203 (12) , 6192-6205
The NRF2/HO- 1 Pathway: a Potential Regulatory Factor in Fluoride-Induced Colonic Injury under Estrogen Deficiency
Our previous studies have demonstrated that fluoride (F) overexposure is a risk factor for colonic microenvironment, yet its underlying mechanisms and the influencing factors remain poorly understood. Here, a rat model of F exposure (0, 25, 50, 100 mg/L in drinking water) combined with ovariectomy (OVX)-induced estrogen deficiency was established to investigate the roles of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway in F-induced colonic damage under the state of estrogen deficiency. Result showed that F exposure significantly reduced occludin and claudin-1 expression, further resulting in the colon’s morphology impairment. Concurrently, F suppressed epithelial proliferation, decreased goblet cell numbers, and diminished short-chain fatty acid (SCFA) production. OVX-induced estrogen deficiency exacerbated F-induced colonic barrier damage and SCFA decreased. Mechanistically, estrogen deficiency aggravated F intestinal toxicity by further inhibiting the protein expression of Nrf2 and HO-1 and upregulating Keap1 protein expression, following downregulated Bcl-2 mRNA levels and upregulated Bax and caspase-3 mRNA levels, and promoting colonic epithelial cell apoptosis. These findings identify that Nrf2/HO-1 key protein disorders are involved in F-induced colonic barrier injury, and estrogen deficiency further aggravated F intestinal toxicity.