Chloroquine regulates the lipopolysaccharide-induced inflammatory response in RAW264.7 cells.

INTRODUCTION AND OBJECTIVES: Macrophage-induced inflammation plays a key role in defense against injury and harmful pathogens. Autophagy and the inflammatory response are associated; however, the relationship between the autophagy pathway and lipopolysaccharide (LPS)- induced inflammatory responses remains unknown. We aimed to determine the effect of autophagy on the LPS-induced myeloid differentiation factor 88 (MyD88)/nuclear transcription factor kB (NF-kB) pathway-mediated inflammatory response in RAW264.7 cells. MATERIALS AND METHODS: To determine the effect of autophagy on the LPS-induced inflammatory response, using various in vitro assays, we determined the effect of autophagy inhibitors and inducers on the inflammatory response in RAW264.7 cells. RESULTS: Chloroquine (CQ), an autophagy inhibitor, suppressed pro-inflammatory cytokines, including interleukin (IL)-1ß, IL-6, and tumor necrosis factor α (TNFα) in LPS-stimulated RAW264.7 cells. CQ also affected inflammatory mediators such as myeloid differentiation factor 88 and NF-kB in LPS-stimulated RAW264.7 cells. CONCLUSION: This study demonstrated that CQ regulates the LPS-induced inflammatory response in RAW264.7 cells. We propose that targeting the regulation of pro-inflammatory cytokine levels and inflammatory mediators using CQ is a promising therapeutic approach for preventing inflammatory injury. CQ serves as a potential therapeutic target for treating various inflammatory diseases.

Effect of Ganoderma lucidum on Cisplatin-induced Nephrotoxicity and Gastrointestinal Toxicity.

BACKGROUND/AIM: Cancer remains a major global health challenge, with an estimated 10 million cancer-related deaths in 2020, hindering efforts to extend life expectancy. Cisplatin, an effective platinum-based chemotherapeutic agent used against various malignancies, has numerous side effects. Ganoderma lucidum is a traditional Chinese medicine with extensive historical use and proven biological activity. This study investigated the effects of G. lucidum on cisplatin-induced nephrotoxicity and gastrointestinal toxicity. MATERIALS AND METHODS: RAW264.7 cells were treated with cisplatin, G. lucidum, or both. Cytotoxicity and antioxidant capacity were measured. Slc:ICR (ICR) mice were treated with cisplatin, G. lucidum, or both. The survival rate and physiological data were measured. RESULTS: G. lucidum suppressed cisplatin-induced cytotoxicity and apoptosis in RAW264.7 cells. G. lucidum suppressed cisplatin-induced nephrotoxicity and gastrointestinal toxicity via its antioxidant effects in ICR mice. CONCLUSION: The suppressive mechanism of G. lucidum may be mediated via its antioxidant effects. These findings indicate its potential to reduce the side effects of cisplatin.