Emodin ameliorates lipopolysaccharide-induced mastitis in mice by inhibiting activation of NF-κB and MAPKs signal pathways.
Emodin is an anthraquinone derivative from the Chinese herb Radix et Rhizoma Rhei. It has been reported that emodin possesses a number of biological properties, such as anti-inflammatory, anti-virus, anti-bacteria, anti-tumor, and immunosuppressive properties. However, the effect of emodin on mastitis is not yet known. The aim of this study was to investigate whether emodin has protective effect against lipopolysaccharide (LPS)-induced mastitis in a mouse model. The mouse model of mastitis was induced by injection of LPS through the duct of mammary gland. Emodin was administered intraperitoneally with the dose of 1, 2, and 4 mg/kg respectively 1h before and 12h after induction of LPS. Emodin significantly reduced infiltration of neutrophilic granulocyte, activation of myeloperoxidase (MPO), concentration of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), mRNA expression levels of TNF-α, IL-1β and IL-6, which were increased in LPS-induced mouse mastitis. In addition, emodin influenced nuclear factor kappa-B signal transduction pathway by inhibiting activation of nuclear transcription factor-kappaB (NF-κB) p65 and degradation inhibitor of NF-κB α (IκBα), and emodin also influenced mitogen activated protein kinases signal transduction pathway by depression activation of p38, extracellular signal-regulated kinase (ERK), and c-jun NH2-terminal kinase (JNK). In conclusion, these results indicated that emodin could exert beneficial effects on experimental mastitis induced by LPS and may represent a novel treatment strategy for mastitis.
Li D
,Zhang N
,Cao Y
,Zhang W
,Su G
,Sun Y
,Liu Z
,Li F
,Liang D
,Liu B
,Guo M
,Fu Y
,Zhang X
,Yang Z
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Baicalein attenuates inflammatory responses by suppressing TLR4 mediated NF-κB and MAPK signaling pathways in LPS-induced mastitis in mice.
Baicalein is a phenolic flavonoid presented in the dry roots of Scutellaria baicalensis Georgi. It has been reported that baicalein possesses a number of biological properties, such as antiviral, antioxidative, anti-inflammatory, antithrombotic, and anticancer properties. However, the effect of baicalein on mastitis has not yet been reported. This research aims to detect the effect of baicalein on lipopolysaccharide (LPS)-induced mastitis in mice and to investigate the molecular mechanisms. Baicalein was administered intraperitoneally 1h before and 12h after LPS treatment. The results indicated that baicalein treatment markedly attenuated the damage of the mammary gland induced by LPS, suppressed the activity of myeloperoxidase (MPO) and the levels of tumor necrosis factor (TNF-α) and interleukin (IL-1β) in mice with LPS-induced mastitis. Besides, baicalein blocked the expression of Toll-like receptor 4 (TLR4) and then suppressed the phosphorylation of nuclear transcription factor-kappaB (NF-κB) p65 and degradation inhibitor of NF-κBα (IκBα) and, and inhibited the phosphorylation of p38, extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK) in mitogen-activated protein kinase (MAPK) signal pathway. These findings suggested that baicalein may have a potential prospect against mastitis.
He X
,Wei Z
,Zhou E
,Chen L
,Kou J
,Wang J
,Yang Z
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Morin alleviates LPS-induced mastitis by inhibiting the PI3K/AKT, MAPK, NF-κB and NLRP3 signaling pathway and protecting the integrity of blood-milk barrier.
Mastitis is a common veterinary clinical disease that restricts the development of dairy farming around the world. Morin, extracted from Mulberry Tree and other herbs, has been reported to possess the function of anti-bacteria, anti-oxidant, and anti-inflammatory. However, whether morin could protect lipopolysaccharide (LPS)-induced mouse mastitis in vivo has not well known. This study firstly aims to evaluate the effects of morin on LPS-induced mouse mastitis in vivo, and then try to illustrate the mechanism involved in the process. Before injected with LPS, mice were intraperitoneally pre-injected with different concentrations of morin, and mice of the control and LPS group were injected with the same amount of saline. Pathologic changes of mammary gland were determined by histopathological examination. Myeloperoxidase (MPO) activities of mammary gland were determined by the MPO kits. The mRNA expressions of inflammatory cytokines including TNF-α, IL-1β and IL-6, and those of chemokine factors CCL2 and CXCL2, and those of tight junctions occludin claudin-3 were examined by qRT-PCR analysis. The activities of IκB, p65, ERK, P38, AKT, PI3K, NLPR3, claudin-1, claudin-3 and occludin were determined by western blotting. The results showed that morin alleviated LPS-induced edema, destructed structures and infiltrated inflammatory cells of mammary gland. Morin administration significantly decreased LPS-induced TNF-α, IL-1β, IL-6, CCL2 and CXCL2 mRNA expressions. Furthermore, western blot analysis also showed that morin significantly reduced LPS-induced phosphorylation of p65, IκB, p38 and ERK, and enhanced LPS-induced phosphorylation of AKT and PI3K. It was also found that LPS-decreased claudin-3 and occludin expressions were also inhibited by morin treatment. In summary, above results suggest that morin indeed protect LPS-induced mouse mastitis in vivo, and the mechanism was through inhibiting the PI3K/AKT, MAPK, NF-κB and NLRP3 signaling pathways and protecting the integrity of blood-milk barrier by regulating the tight junction proteins expressions.
Jiang A
,Zhang Y
,Zhang X
,Wu D
,Liu Z
,Li S
,Liu X
,Han Z
,Wang C
,Wang J
,Wei Z
,Guo C
,Yang Z
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