Cyanidin-3-O-β-glucoside inhibits lipopolysaccharide-induced inflammatory response in mouse mastitis model

Abstract

bacteria are the most frequent causative agents of severe mastitis ( 2 ). Lipopolysaccharide (LPS), a main component of the outer membrane of gram-negative bacteria, has been identifi ed as an important risk factor for mastitis ( 3 ). Tolllike receptor (TLR4) is the main receptor of LPS ( 4 ). Upon stimulation by LPS, TLR4 is recruited to lipid rafts and interacts with its adaptor molecules, resulting in nuclear factor-B (NF-B) and interferon regulatory factor 3 (IRF3) activation and cytokine production ( 5 ).The liver X receptors (LXRs) are nuclear receptors that play central roles in the transcriptional control of lipid metabolism. Activation of LXRs induces expression of genes involved in cholesterol effl ux, such as ABCA1 and ABCG1 ( 6 ). In addition to their function in lipid metabolism, LXRs have also been found to play an important role in infl ammatory responses ( 7 ). Reports have shown that synthetic LXR agonists promote cholesterol effl ux (the effl ux of cholesterol from cells and total cell cholesterol, membrane cholesterol, and lipid raft cholesterol all go down) and inhibit infl ammation ( 8 ). ABCA1 and ABCG1 are members of the ABC superfamily of transmembrane transporters that pump specifi c substrates across membranes ( 9 ). Both the ABCG1 and ABCA1 genes are expressed in numerous tissues and are highly activated by the nuclear receptor LXR. Activation of ABCA1 and ABCG1 can induce cholesterol effl ux from the cell and downregulate lipid raft cholesterol levels ( 10 ). Lipid rafts are microdomains of the plasma membrane which are enriched in cholesterol and sphingolipids. They serve as a platform for signal transduction ( 11 ). Treatment with raft-disrupting drugs can inhibit the LPS-induced infl ammatory response ( 12, 13 ). Mastitis is a highly prevalent and important infectious disease and is responsible for severe production effects. Milk yield and composition can be affected, which results in impaired infant growth and development ( 1 ). Gram-negative This work was supported by grants from the National Natural Science Foundation of China (30972225 and 30771596) Abbreviations: C3G, cyanidin-3-O-␤ -glucoside; DEX, dexamethasone; GM1, Ganglioside M1; IL, interleukin; IRF3, interferon regulatory factor 3; LPS, lipopolysaccharide; LXR, liver X receptor; mAb, monoclonal Ab; M ␤ CD, methyl-␤ -cyclodextrin; MMEC, mouse mammary epithelial cell; MPO, myeloperoxidase; MTT, 3-(4,5-dimethylthiazol-2-y1)-2,5-diphenyltetrazolium bromide; NF-B, nuclear factor-B; OD, optical density; RANTES, regulated upon activation normal T-cell expressed and secreted; TLR4, toll-like receptor 4 .

Baicalein attenuates inflammatory responses by suppressing TLR4 mediated NF-κB and MAPK signaling pathways in LPS-induced mastitis in mice

“…Curcumin attenuates inflammatory responses by suppressing TLR4 signaling pathways [30]. Cyaniding-3-O-β-glucoside inhibits inflammatory responses by regulating liver X receptor (LXR) [13]. Baicalein inhibits inflammatory responses by reductions in TLR2 signaling pathways [31].…”

“…Cytokines such as TNF-α and IL-1β play a key role in inflammatory diseases [11][12][13]. To determine whether the inflammatory cytokines mRNA expression was influenced by baicalein, RT-PCR was carried out to measure the mRNA levels of TNF-α and IL-1β (Fig.…”

7‐Dehydrocholesterol (7‐DHC), But Not Cholesterol, Causes Suppression of Canonical TGF‐β Signaling and Is Likely Involved in the Development of Atherosclerotic Cardiovascular Disease (ASCVD)

“…DMSO has been shown to ameliorate atherosclerosis in animal models [Huang et al, ]. Many agents or compounds which are known to reduce the risk of ASCVD have been found to exhibit TGF‐β enhancer activity [Fu et al, ; Huang et al, , ,].…”

Cyanidin-3-O-glucoside Ameliorates Postprandial Hyperglycemia in Diabetic Mice

“…The molecular formula of C3G is C21H21O11+, and its molar mass is 449.3843 g/mol. C3G has the ability to stimulate insulin secretion from pancreatic cells in the presence of 4 mM or 10 mM glucose [25] and has also been reported to have anti-inflammatory and antioxidant effects [8,28]. Despite these studies, there is no experimental data demonstrating a relationship between postprandial blood glucose levels and C3G.…”