Gambogic acid alleviates inflammation and apoptosis and protects the blood-milk barrier in mastitis induced by LPS

PK/PD Modeling to Assess Rifaximin Clinical Dosage in a Mouse Model of Staphylococcus aureus-Induced Mastitis

“…In the pilot study of rifaximin in mammary gland, the concentration of rifaximin of the untreated mammary gland homogenate was lower than or equal to the limit of quantitation, which is consistent with the blood-milk barrier ( 4 ). The blood-milk barrier is formed by mammary gland secretory cells that are closely linked together at their apex by tight junctions, which helps prevent the selective diffusion of drugs between the blood and mammary gland ( 38 , 39 ). Therefore, the PK parameters in the mammary gland were used for the PK/PD model and Monte Carlo simulation to evaluate and develop a rational regimen for clinical administration of rifaximin.…”

Gambogic acid protects LPS-induced apoptosis and inflammation in a cell model of neonatal pneumonia through the regulation of TrkA/Akt signaling pathway

“…The results from both TUNEL assay and western blot assay demonstrated that, GA significantly reduced apoptosis and inflammatory protein biomarkers in LPS-injured WI-38 cells. In a very recent study, Tang and colleagues demonstrated that GA could alleviate inflammation and apoptosis and protect the blood-milk barrier in mastitis [ 13 ]. However, before our work, the anti-apoptosis and anti-inflammation effects of GA has never been reported in any studies related to neonatal pneumonia.…”

“…This data not only supported the findings in previous publications showing the inflammation-suppressing effect of Akt [ 22 , 23 ], but also suggested that the anti-cytotoxic mechanism of GA in LPS-treated WI-38 cells was very likely through the Akt signaling pathway. In the recent study in mastitis, it was demonstrated that GA protected the blood-milk barrier and alleviated inflammation / apoptosis by regulating the nuclear factor kappaB (NF-kappaB) signaling pathway [ 13 ]. In addition, GA-induced TrkA activation was shown to be correlated with osteoblastic differentiation [ 11 ].…”

“…Moreover, GA has been demonstrated to protect neuronal death through neurotrophic signaling pathway as well as activating tropomyosin receptor kinase A (TrkA) receptor [ 12 ]. Specifically, a recent study showed that GA had markedly anti-inflammatory and anti-apoptosis activities in lipopolysaccharide (LPS)-induced mastitis [ 13 ]. However, any possible molecular mechanisms of GA in human neonatal pneumonia have never been elucidated.…”

“…In the present study, we established an in vitro cellular model of human neonatal pneumonia, in which a human lung fibroblast cell line, WI-38 cells were cultured in vitro and treated with LPS to induce neonatal pneumonia-like inflammation and apoptosis among WI‐38 cells [ 13 – 18 ]. We then pre-incubated WI‐38 cells with various concentration of GA to observe the potential anti-inflammatory and anti-apoptosis effects of GA on LPS-induced cytotoxicity.…”