Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1248/cpb.25.2959 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
FSH exacerbates bone loss by promoting osteoclast energy metabolism through the CREB-MDH2-NAD axis.
Metabolism
January 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan 430079, PR China. Electronic address:
Aims: Osteoclast energy metabolism is a promising target for treating diseases characterized by high osteoclast activity, such as osteoporosis. However, the regulatory factors involved in osteoclast bioenergetic processes are still in the early stages of being fully understood. This study reveals the effects of follicle-stimulating hormone (FSH) on osteoclast energy metabolism.
View Article and Find Full Text PDFTrametes robiniophila Murr. extract alleviates influenza-induced lung injury by regulating gut microbiota and metabolites.
J Pharm Biomed Anal
January 2025
School of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250355, China; State Key Laboratory of Microbial Technology, Shandong University, Qingdao 266237, China. Electronic address:
Trametes robiniophila Murr. (Huaier) is a traditional medicinal fungus known for its pharmacological properties, including heat-clearing, detoxifying, anti-inflammatory, and antitumor effects. Our previous research has demonstrated its antiviral activity, but the exact therapeutic mechanisms remain unclear.
View Article and Find Full Text PDFGinkgolide B regulates apoptosis, oxidative stress, and mitochondrial dysfunction in MPP-induced SK-N-SH cells by targeting HDAC4/JNK pathway.
Naunyn Schmiedebergs Arch Pharmacol
January 2025
Huai'an Hospital Affiliated to Yangzhou University, The Fifth People's Hospital of Huai'an), 1 Huaihe East Road, Huaiyin District, Huai'an City, Jiangsu Province, China.
Ginkgolide B (GB) is a bioactive constituent found in Ginkgo biloba leaves that has been long recognized as a protective agent against many neurological disorders. Our study aimed to examine the effect of GB in an in vitro Parkinson's disease (PD) model and to investigate its neuroprotective mechanism as a primary objective. SK-N-SH cells were challenged with 1-methyl-4-phenylpyridinium (MPP) to act as a PD-like model of neuronal damage.
View Article and Find Full Text PDFSorafenib enhanced the function of myeloid-derived suppressor cells in hepatocellular carcinoma by facilitating PPARα-mediated fatty acid oxidation.
Mol Cancer
January 2025
Department of Radiation Oncology, Peking University Third Hospital, Beijing, 100191, China.
Background: Sorafenib, an FDA-approved drug for advanced hepatocellular carcinoma (HCC), faces resistance issues, partly due to myeloid-derived suppressor cells (MDSCs) that enhance immunosuppression in the tumor microenvironment (TME).
Methods: Various murine HCC cell lines and MDSCs were used in a series of in vitro and in vivo experiments. These included subcutaneous tumor models, cell viability assays, flow cytometry, immunohistochemistry, and RNA sequencing.
Relationships between nutritional status and serum adipokine levels with chemotherapy efficacy in late-stage colorectal cancer patients.
Int J Colorectal Dis
January 2025
Department of Infectious Diseases (Hepatology), Affiliated Hospital of Shaoxing University, 999 Zhongxing South Road, Shaoxing, 312000, Zhejiang, China.
Objective: Colorectal cancer (CRC) is a common cancer, with chemotherapy as its major therapy. Nutritional status (NS) and adipokines implicated in CRC. We explored the impacts of NS indicators (hemoglobin, albumin, and prealbumin) and serum adipokine (visfatin, adiponectin, and resistin) level on chemotherapy efficacy in late-stage CRC patients.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!