L., commonly known as cocoa, has been an integral part of human culture and diet for thousands of years. However, recent scientific research has highlighted its potential therapeutic properties, particularly in the treatment of cancer and inflammatory diseases. This comprehensive review analyzes the anti-inflammatory and anticancer effects of extracts combined with nanoparticles using in vitro and in vivo studies. Its diverse biological activity can be attributed to its rich phytochemical profile, including polyphenols, flavonoids, and alkaloids. In vitro studies have found that cocoa extracts, alone or in combination with nanoparticles, inhibit cancer cell proliferation, induce apoptosis and modulate key signaling pathways in various cancer cell lines. The extracts have also been found to reduce tumor growth and enhance the efficacy of conventional chemotherapeutic agents, potentially reducing their side effects, in vivo. Its anti-inflammatory properties are based on its ability to modulate inflammatory mediators, inhibit NF-κB signaling, and regulate macrophage polarization. These effects have been observed in both cellular and animal models of inflammation. This review opens up new possibilities for future research and therapeutic applications, highlighting the potential of as a valuable complementary approach in the treatment and prevention of cancer and inflammatory diseases.
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http://dx.doi.org/10.3390/antiox13111376 | DOI Listing |
Breast Cancer Res
January 2025
Division of Medical Oncology, The Ohio State University Comprehensive Cancer Center, Columbus, OH, USA.
Background: Epidemiological studies associate an increase in breast cancer risk, particularly triple-negative breast cancer (TNBC), with lack of breastfeeding. This is more prevalent in African American women, with significantly lower rate of breastfeeding compared to Caucasian women. Prolonged breastfeeding leads to gradual involution (GI), whereas short-term or lack of breastfeeding leads to abrupt involution (AI) of the breast.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
School of Medicine, Chinese PLA General Hospital, Nankai University, Beijing, China.
Background: Glioblastoma multiforme (GBM) exhibits a cellular hierarchy with a subpopulation of stem-like cells known as glioblastoma stem cells (GSCs) that drive tumor growth and contribute to treatment resistance. NAD(H) emerges as a crucial factor influencing GSC maintenance through its involvement in diverse biological processes, including mitochondrial fitness and DNA damage repair. However, how GSCs leverage metabolic adaptation to obtain survival advantage remains elusive.
View Article and Find Full Text PDFEur J Med Res
January 2025
Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310000, China.
Objectives: SOX10 is crucially implicated in various cancer, yet the regulatory role in pancreatic cancer (PC) remains enigmatic. Underlying molecular mechanisms of SOX10 in PC were explored in our study.
Methods: Relationships between SOX10 and immune landscape were estimated using bioinformatic approaches.
Chin Med
January 2025
Department of Clinical Chinese Pharmacy, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, 102488, China.
Background: With extended gefitinib treatment, the therapeutic effect in some non-small cell lung cancer (NSCLC) patients declined with the development of drug resistance. Aidi injection (ADI) is utilized in various cancers as a traditional Chinese medicine prescription. This study explores the molecular mechanism by which ADI, when combined with gefitinib, attenuates gefitinib resistance in PC9GR NSCLC cells.
View Article and Find Full Text PDFMol Med
January 2025
Department of Gastroenterology and Medical Research Center, Liaoning Key Laboratory of Research and Application of Animal Models for Environmental and Metabolic Diseases, ShengJing Hospital of China Medical University, SanHao Street No. 36, HePing District, Shenyang, 110000, Liaoning, China.
The lack of knowledge about the mechanism of hyperoxia-induced intestinal injury has attracted considerable attention, due to the potential for this condition to cause neonatal complications. This study aimed to explore the relationship between hyperoxia-induced oxidative damage and ferroptosis in intestinal tissue and investigate the mechanism by which hyperoxia regulates inflammation through ferroptosis. The study systematically evaluated the effects of hyperoxia on oxidative stress, mitochondrial damage, ferroptosis, and inflammation of intestinal epithelial cells both in vitro and in vivo.
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