Ocotillol-Type Pseudoginsenoside-F11 Alleviates Lipopolysaccharide-Induced Acute Kidney Injury through Regulation of Macrophage Function by Suppressing the NF-κB/NLRP3/IL-1β Signaling Pathway-Reference-Cited by-同舟云学术

Ocotillol-Type Pseudoginsenoside-F11 Alleviates Lipopolysaccharide-Induced Acute Kidney Injury through Regulation of Macrophage Function by Suppressing the NF-κB/NLRP3/IL-1β Signaling Pathway

Published:2024-09-06 Issue: Volume: Page:
ISSN:0021-8561
Container-title:Journal of Agricultural and Food Chemistry
language:en
Short-container-title:J. Agric. Food Chem.

Author:

Wang Yaru¹,Zhang Jinyu¹,Yang Zhuo²,Li Changcheng¹,Zhang Chenming³,Sun Shengkai²,Jiao Ziyan²,Che Guanghua²,Gao Hang¹,Liu Jinping⁴^ORCID,Li Jing¹^ORCID

Affiliation:

1. Innovation Center of New Drug Preclinical Pharmacology Evaluation of Jilin Province, Department of pharmacology, College of Basic Medicine of Jilin University, Changchun, Jilin 130012, China

2. The Second Norman Bethune Hospital of Jilin University, Changchun, Jilin 130062, China

3. China-Japan Union Hospital of Jilin University, Changchun, Jilin 130022, China

4. Research Center of Natural Drug, School of Pharmaceutical Sciences of Jilin University, Changchun, Jilin 130012, China

Funder

Jilin Provincial Key Research and Development Plan Project

Jilin University

Jilin Provincial Scientific and Technological Development Program

Publisher

American Chemical Society (ACS)

Link

https://pubs.acs.org/doi/pdf/10.1021/acs.jafc.4c05185

Reference45 articles.

1. Acute Kidney Injury Epidemiology: From Recognition to Intervention

2. Acute kidney injury from sepsis: current concepts, epidemiology, pathophysiology, prevention and treatment

3. Precisely Regulating M2 Subtype Macrophages for Renal Fibrosis Resolution

4. Erratum: Snail1-induced partial epithelial-to-mesenchymal transition drives renal fibrosis in mice and can be targeted to reverse established disease.

5. [Corrigendum] HMGB1 participates in LPS‑induced acute lung injury by activating the AIM2 inflammasome in macrophages and inducing polarization of M1 macrophages via TLR2, TLR4, and RAGE/NF‑κB signaling pathways