The American journal of Chinese medicine
-
Acupuncture and moxibustion are widely acknowledged as effective complementary therapies for managing inflammatory bowel disease (IBD) in traditional Chinese medicine. However, the regulatory mechanisms by which these two therapies exert their therapeutic effects in IBD are yet to be fully elucidated. The objective of this study was to investigate the mechanisms of action underlying acupuncture and moxibustion and the regulative differences between them as therapeutic interventions for IBD. ⋯ Acupuncture and moxibustion had distinct effects on the regulation of the intestinal microbiota and metabolic pathways in IBD mice. Moxibustion regulated a greater number of metabolic pathways than acupuncture, the majority of which were associated with amino acid metabolism, brain signal transmission, energy metabolism, and anti-inflammatory pathways. These findings provide a scientific basis for the differential applications of acupuncture and moxibustion in clinical practice.
-
Fucoxanthin, sourced from marine brown algae, diatoms, and microalgae, is known to possess strong anti-inflammatory activity. To explore its intrinsic mechanism, we investigated its effects on acute lung injury (ALI) with an experiment using lipopolysaccharide (LPS)-induced RAW264.7 inflammatory cells and an ALI animal model. Fucoxanthin was observed to suppress the inflammatory response in vitro by reducing the levels of inflammatory markers such as PTGS2, iNOS, and TNF-α. ⋯ Further research revealed that fucoxanthin could raise the levels of [Formula: see text]-Glu-Cys and carbamyl glycine, which are intermediate metabolites of glutathione synthesis, in RAW264.7 cells. This implies that fucoxanthin can inhibit ferroptosis by regulating the [Formula: see text]-glutamyl cycle. Our research demonstrated that fucoxanthin is capable of activating phosphorylated STAT3 and raising the expression of Nrf2 and HO-1, implying that fucoxanthin may be able to prevent LPS-induced ferroptosis in ALI through the Nrf2/STAT3 pathway.
-
Panax notoginseng saponins (PNS), the primary medicinal ingredient of Panax notoginseng, mitigates cerebral ischemia-reperfusion injury (CIRI) by inhibiting inflammation, regulating oxidative stress, promoting angiogenesis, and improving microcirculation. Moreover, PNS activates nuclear factor erythroid 2-related factor 2 (Nrf2), which is known to inhibit ferroptosis and reduce inflammation in the rat brain. However, the molecular regulatory roles of PNS in CIRI-induced ferroptosis remain unclear. ⋯ Mechanistically, PNS treatment facilitated Nrf2 activation, thereby regulating the expression of iron overload and lipid peroxidation-related proteins and the activities of anti-oxidant enzymes. This cascade inhibited ferroptosis and mitigated CIRI. Altogether, these results suggest that the ferroptosis-mediated activation of Nrf2 by PNS reduces inflammation and is a promising therapeutic approach for CIRI.
-
Acute kidney injury (AKI) is a major public health problem worldwide that still lacks effective treatments. Recent studies have suggested that ferroptosis is a key mediator of AKI due to its activation of lipid peroxidation. Therefore, we hypothesized that antiferroptosis agents might be a novel potential therapeutic strategy for AKI. ⋯ Moreover, knockdown of VKORC1 diminished the renal protective and antiferroptosis roles of LG. Collectively, our findings demonstrated that LG protected against AKI by inhibiting VKORC1-mediated ferroptosis. This suggests that inhibiting ferroptosis might be a novel therapeutic approach in the future.
-
Diabetic kidney disease (DKD) has become the primary cause of end-stage renal disease (ESRD), causing an urgent need for preventive strategies for DKD. Astragaloside I (ASI), a bioactive saponin extracted from Astragalus membranaceus (Fisch.) Bunge has been demonstrated to possess a variety of biological activities. This study investigates the therapeutic potential of ASI in DKD and the underlying molecular mechanism using db/db mice in vivo and high glucose (HG)-induced SV40-MES-13 cells in vitro. ⋯ Furthermore, ASI downregulated HDAC3 expression, upregulated Klotho expression, and enhanced Klotho release. ASI is directly bound to HDAC3, and the beneficial effects of ASI on Klotho/TGF-β1/Smad2/3-mediciated renal fibrosis in DKD were reversed by the HDAC3 agonist ITSA-1. In conclusion, ASI attenuates renal fibrosis in DKD, and may act through concurrently inhibiting HDAC3 and TGF-β1, thereby regulating HDAC3-mediciated Klotho/TGF-β1/Smad2/3 pathway.