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Amelioration of radiation-induced liver damage by p-coumaric acid in mice
Yun-Hong Li,Jiang-Xue Wu,Qian He,Jia Gu,Lin Zhang,Hao-Zhi Niu,Xin-Wen Zhang,Han-Ting Zhao,Jia-Ying Xu,Li-qiang Qin 한국식품과학회 2022 Food Science and Biotechnology Vol.31 No.10
Radiation-induced liver damage (RILD) is a spiny problem in radiotherapy or other circumstances that exposure to radiation. The need for radioprotective agent is increasing to protect liver tissue. This study aimed to explore the hepatoprotective effect of p-coumaric acid (CA) against RILD. C57BL/6 male mice were exposed to 4 Gy irradiation and administrated with CA for 4 days starting on the same day of irradiation. Mice were sacrificed to obtain blood and liver tissues on day 3.5 or 14 post irradiation, respectively. The blood and liver tissues were collected. As compared with the only irradiated group, CA supplementation improved liver morphology, decreased serum alanine aminotransferase and aspartate aminotransferase, inhibited BCL2-associated X (BAX) protein expression, and improved the mice hematopoietic function. CA at the dose of 100 mg/kg body weight showed better effect compared to the other doses. Thus, CA might possess potential to protect against RILD.
Correction to: Amelioration of radiation‑induced liver damage by p-coumaric acid in mice
Yun-Hong Li,Jiang-Xue Wu,Qian He,Jia Gu,Lin Zhang,Hao-Zhi Niu,Xin-Wen Zhang,Han-Ting Zhao,Jia-Ying Xu,Li-qiang Qin 한국식품과학회 2023 Food Science and Biotechnology Vol.32 No.5
In the original publication, incorrect versions of Figs. 2 , 3 ,4 and 5 were published. Specifi cally, the arrows in Figs. 2 , 3and 4 were moved outside the representative images, and theFig. 5 was wrongly replaced by another fi gure. The correctversion of Figs. 2 , 3 , 4 , and 5 , were shown below.
Yan Wang,Zhi-yun Niu,Yu-jie Guo,Li-hua Wang,Feng-ru Lin,Jing-yu Zhang 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Hematopoietic stem cell (HSC) transplantation could be of therapeutic value for aplastic anemia (AA) patients, and immunosuppressants may facilitate the efficiency of the procedure. As anti-inflammatory cytokine interleukin-11 (IL-11) has a thrombopoietic effect, its use in cases of chronic bone marrow failure, such as AA, has been proposed to induce HSC function. However, the putative mechanisms that may support this process remain poorly defined. We found that decreased miR-204-5p levels were coincident with increased proliferation in mouse HSCs following exposure to IL-11 in vitro. Through inhibiting NF-кB activity, miR-204-5p repression was demonstrated to be a downstream effect of IL-11 signaling. miR-204-5p was shown to directly target thrombopoietin (TPO) via sequence-dependent 3′-UTR repression, indicating that this microRNA-dependent pathway could serve an essential role in supporting IL-11 functions in HSCs. Increased TPO expression in HSCs following IL-11 exposure could be mimicked or blocked by inhibiting or overexpressing miR-204-5p, respectively. Consistent with these in vitro findings, IL-11 promoted HSC engraftment in a mouse model of AA, an effect that was attenuated in cells overexpressing miR-204-5p. The reduction in miR-204-5p levels is an integral component of IL-11 signaling that may play an essential role in treating AA.