Abstract:The immuno therapeutic potential of hydro-methanolic extract of Azadirachta indica (A. indica) was studied during bovine clinical mastitis (CM). The somatic cell count (SCC), total bacterial count (TBC), milk differential leukocyte count (DLC), hydrogen peroxide (H(2)O(2)), superoxide anion (O(2) (-)) production and interleukin- 2 (IL-2) and gamma interferon (IFN-gamma) cytokines expression were studied before and after intramammary infusion of A. indica extract in diseased cows. The results revealed that A. i… Show more
“…It has been demonstrated that LPS can effectively induce mastitis in mouse and bovine models [23][24][25]. LPS can induce the production of cytokines, and these cytokines can amplify the inflammatory response in mastitis [26]. It has been suggested that TNF-a, IL-1b, IL-6 and RANTES play an important role in mastitist pathogenesis [27].…”
Glycyrrhizin, a triterpene glycoside isolated from licorice root, is known to have anti-inflammatory activities. However, the effect of glycyrrhizin on mastitis has not been reported. The purpose of this study was to investigate the anti-inflammatory effect and mechanism of action of glycyrrhizin on lipopolysaccharide (LPS)-induced mastitis in mouse. An LPS-induced mouse mastitis model was used to confirm the anti-inflammatory activity of glycyrrhizin in vivo. Primary mouse mammary epithelial cells were used to investigate the molecular mechanism and targets of glycyrrhizin. In vivo, glycyrrhizin significantly attenuated the mammary gland histopathological changes, myeloperoxidase activity and infiltration of neutrophilic granulocytes and downregulated the expression of tumor necrosis factor-a, interleukin (IL)-1b and IL-6 caused by LPS. In vitro, glycyrrhizin dose-dependently inhibited the LPS-induced expression of tumor necrosis factor-a, IL-6, and RANTES. Western blot analysis showed that glycyrrhizin suppressed LPS-induced nuclear factor-jB and interferon regulatory factor 3 activation. However, glycyrrhizin did not inhibit nuclear factor-jB and interferon regulatory factor 3 activation induced by MyD88-dependent (MyD88, IKKb) or TRIF-dependent (TRIF, TBK1) downstream signaling components. Moreover, glycyrrhizin did not act though affecting the function of CD14 or expression of Toll-like receptor 4. Finally, we showed that glycyrrhizin decreased the levels of cholesterol of lipid rafts and inhibited the translocation of Toll-like receptor 4 to lipid rafts. Moreover, glycyrrhizin activated ATP-binding cassette transporter A1, which could induce cholesterol efflux from lipid rafts. In conclusion, we find that the antiinflammatory effects of glycyrrhizin may be attributable to its ability to activate ATP-binding cassette transporter A1. Glycyrrhizin might be a useful therapeutic reagent for the treatment of mastitis and other inflammatory diseases.
“…It has been demonstrated that LPS can effectively induce mastitis in mouse and bovine models [23][24][25]. LPS can induce the production of cytokines, and these cytokines can amplify the inflammatory response in mastitis [26]. It has been suggested that TNF-a, IL-1b, IL-6 and RANTES play an important role in mastitist pathogenesis [27].…”
Glycyrrhizin, a triterpene glycoside isolated from licorice root, is known to have anti-inflammatory activities. However, the effect of glycyrrhizin on mastitis has not been reported. The purpose of this study was to investigate the anti-inflammatory effect and mechanism of action of glycyrrhizin on lipopolysaccharide (LPS)-induced mastitis in mouse. An LPS-induced mouse mastitis model was used to confirm the anti-inflammatory activity of glycyrrhizin in vivo. Primary mouse mammary epithelial cells were used to investigate the molecular mechanism and targets of glycyrrhizin. In vivo, glycyrrhizin significantly attenuated the mammary gland histopathological changes, myeloperoxidase activity and infiltration of neutrophilic granulocytes and downregulated the expression of tumor necrosis factor-a, interleukin (IL)-1b and IL-6 caused by LPS. In vitro, glycyrrhizin dose-dependently inhibited the LPS-induced expression of tumor necrosis factor-a, IL-6, and RANTES. Western blot analysis showed that glycyrrhizin suppressed LPS-induced nuclear factor-jB and interferon regulatory factor 3 activation. However, glycyrrhizin did not inhibit nuclear factor-jB and interferon regulatory factor 3 activation induced by MyD88-dependent (MyD88, IKKb) or TRIF-dependent (TRIF, TBK1) downstream signaling components. Moreover, glycyrrhizin did not act though affecting the function of CD14 or expression of Toll-like receptor 4. Finally, we showed that glycyrrhizin decreased the levels of cholesterol of lipid rafts and inhibited the translocation of Toll-like receptor 4 to lipid rafts. Moreover, glycyrrhizin activated ATP-binding cassette transporter A1, which could induce cholesterol efflux from lipid rafts. In conclusion, we find that the antiinflammatory effects of glycyrrhizin may be attributable to its ability to activate ATP-binding cassette transporter A1. Glycyrrhizin might be a useful therapeutic reagent for the treatment of mastitis and other inflammatory diseases.
“…Inflammation is also considered to be a characteristic of many human diseases, such as diabetes, cardiovascular disorders, cancers, and arthritis [4]. Most of the important signaling pathways, including the TLR4/MYD88 pathway, PI3K-AKT pathway, MAPK pathway, NF-jB pathway, and the TNF pathway, are all related to inflammation regulation [5][6][7][8].…”
Swertiamarin (SW), a representative component in Flos Lonicerae Japonicae, has been reported to exert significant activity in preventing infections. In this research, we aim to clarify the details of SW and its target to explore SW's underlying anti-inflammatory mechanisms. An azide labeled SW probe was synthesized for protein target fishing, and the results demonstrated that AKT could be captured specifically. Immunofluorescence colocalization with AKT was implemented by a click reaction of the SW probe and alkynyl CY5. The result showed that AKT was one of the targets of SW. Then, a competitive combination experiment using a set of AKT inhibitors and a membrane translocation experiment confirmed that SW might target the pleckstrin homology (PH) domain of AKT. This specific binding directly deactivated the phosphorylation of AKT on both Ser473 and Thr308, which induced the dephosphorylation of IKK and NF-jB. Finally, proinflammatory cytokines (TNF-a, IL-6, and IL-8) were suppressed both in cells and in acute lung injury animal model by targeting AKT-PH domain. This study demonstrated that SW functions as a natural AKT inhibitor and presents significant anti-inflammatory activity by directly regulating the AKT-PH domain and inhibiting downstream inflammatory molecules.
“…Reduced phagocytic activity and production of reactive oxygen species by milk cells after parturition has been described to correlate with a negative metabolic and energy balance that directly affects neutrophil function and increases the risk of mastitis in dairy cows (Cai et al 1994;Hoeben et al 2000). Similar findings were also observed in bovine mastitis (Mukherjee et al 2005;De and Mukherjee 2009). However, phagocytic activity (42.20%), hydrogen peroxide production (29.46%) and myeloperoxidase (49.27%) enzyme activity increased significantly (P < 0.05) in subclinical mastitis-infected quarters following intramammary treatment with amoxicillin plus sulbactam.…”
ABSTRACT:The therapeutic potential of amoxicillin plus sulbactam and its effect on dynamics of milk leukocytes in bovine sub clinical mastitis were investigated in this study. Therapeutic efficacy was measured by somatic cell count and total bacterial count of the milk, whereas, the dynamics of milk leukocytes were assessed by measuring phagocytosis, hydrogen peroxide production, myeloperoxidase and lactoperoxidase enzyme levels in the milk leukocytes. Forty-five crossbred cows were randomly divided into three equal groups. Group I consisting of 15 cows served as healthy control, whereas 30 cows (sub clinical mastitis) were randomly divided into Groups II and III on the basis of positive reactions in the California Mastitis Test. Group II cows received 300mg of amoxicillin plus sulbactam twice daily for three days and Group III received sterile 5 ml phosphate buffer saline (pH 7.4) for three days. Both treatments were administered via the intramammary route. Observations were made up to 15 days after initiation of treatment. The results revealed a pronounced drop in somatic cell count and total bacterial count, whereas significant (P < 0.05) enhancement of phagocytic activity (42.20%), hydrogen peroxide production (29.46%), myeloperoxidase (49.27%) and lactoperoxidase (147.10%) enzyme levels in the milk leukocytes in Group II cows during post treatment periods were observed. Such changes were statistically non-significant in Group III cows. The results of the present study indicate that intramammary use of amoxicillin plus sulbactam augments the bactericidal function of milk leukocytes during bovine sub clinical mastitis and demonstrate the strong therapeutic potential against bovine subclinical mastitis.
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