Chinese herbal Jin-Ying-Tang attenuates the inflammatory response by inhibiting the activation of TLR4/MyD88/TRAF-6/NIK pathway at the mRNA level in LPS-stimulated mouse mammary epithelial cells

Introduction: The effects of Jin-Ying-Tang (JYT) on Toll-like Receptor 4 (TLR4) signalling transduction of lipopolysaccharide (LPS)-stimulated mouse mammary epithelial cells (MECs) in vitro were examined. Material and Methods: The cytotoxicity of JYT (0.06-62.50 mg/mL) on mouse MECs was determined by MTT assay. The MECs were co-cultured with LPS in the presence or absence of JYT (39.10 mu g/mL, 391 mu g/mL, 3910 mu g/mL). The concentrations of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) in the culture supernatants were detected by ELISA. The mRNA expression of TLR4 and downstream TLR4 signalling molecules such as myeloid differentiation factor 88 (MyD88), tumour necrosis factor receptor associated factor 6 (TRAF-6), inhibitor kappa B (I kappa B), and nuclear factor.B inducing kinase (NIK) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Results: The results showed that the IC50 of JYT on MECs was 12.25 mg/mL and JYT could significantly decrease the concentrations of IL-6 and TNF-alpha in LPS-stimulated MECs (P < 0.05). The mRNA expression of TLR4, MyD88, TRAF-6, I kappa B, and NIK was also significantly decreased when the LPS-stimulated MECs were cocultured at appropriate concentrations of JYT (P < 0.05, P < 0.01). Conclusion: These observations indicate a potential mechanism through which JYT attenuates the systemic inflammatory response to LPS-stimulated mouse mammary epithelial cells by inhibiting the activation of TLR4/MyD88/TRAF-6/NIK pathway at the mRNA level

Chinese herbal Jin-Ying-Tang attenuates the inflammatory response by inhibiting the activation of TLR4/MyD88/TRAF-6/NIK pathway at the mRNA level in LPS-stimulated mouse mammary epithelial cells

Introduction: The effects of Jin-Ying-Tang (JYT) on Toll-like Receptor 4 (TLR4) signalling transduction of lipopolysaccharide (LPS)-stimulated mouse mammary epithelial cells (MECs) in vitro were examined. Material and Methods: The cytotoxicity of JYT (0.06-62.50 mg/mL) on mouse MECs was determined by MTT assay. The MECs were co-cultured with LPS in the presence or absence of JYT (39.10 mu g/mL, 391 mu g/mL, 3910 mu g/mL). The concentrations of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) in the culture supernatants were detected by ELISA. The mRNA expression of TLR4 and downstream TLR4 signalling molecules such as myeloid differentiation factor 88 (MyD88), tumour necrosis factor receptor associated factor 6 (TRAF-6), inhibitor kappa B (I kappa B), and nuclear factor.B inducing kinase (NIK) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Results: The results showed that the IC50 of JYT on MECs was 12.25 mg/mL and JYT could significantly decrease the concentrations of IL-6 and TNF-alpha in LPS-stimulated MECs (P < 0.05). The mRNA expression of TLR4, MyD88, TRAF-6, I kappa B, and NIK was also significantly decreased when the LPS-stimulated MECs were cocultured at appropriate concentrations of JYT (P < 0.05, P < 0.01). Conclusion: These observations indicate a potential mechanism through which JYT attenuates the systemic inflammatory response to LPS-stimulated mouse mammary epithelial cells by inhibiting the activation of TLR4/MyD88/TRAF-6/NIK pathway at the mRNA level

Efficacy of combined glucocorticoid and hyperbaric oxygen therapy against delayed encephalopathy after carbon monoxide poisoning, and its effect on expression of immune-associated cytokines

Purpose: To study the efficacy of glucocorticoid combined with hyperbaric oxygen therapy for the treatment of delayed encephalopathy after carbon monoxide poisoning (DEACMP), and its effect on the expression of immune-associated cytokines.Methods: A total of 102 DEACMP patients in PLA General Hospital, Haidian, China were divided into two groups of 51 patients each, namely, observation group (glucocorticoid + hyperbaric oxygen therapy), and control group (hyperbaric oxygen only). The clinical data for each group was retrospectively analyzed. Clinical efficacy, improvement time, hospitalization time, cognitive function, activities associated with daily living, changes in immunity-associated cytokines, and incidence of adverse reactions were compared for the two groups.Results: Following treatment, the time taken for improvement, duration of hospitalization, cognitive function, daily living activity and total effectiveness in the observation group were significantly higher than those for the control group (p &lt; 0.05). In addition, the levels of transforming growth factor beta 1 (TGF- β1), interleukin 4 (IL-4) and interferon-gamma (IFN-γ) in the observation group were significantly greater than for the corresponding control group levels (p &lt;0.05). There was no significant difference in incidence of adverse reactions between the two groups (p &gt; 0.05).Conclusion: These results suggest that a combination therapy of glucocorticoid and hyperbaric oxygen therapy for the treatment of DEACMP is more eutherapeutic in the improvement of cognitive function and activities of daily living in DEACMP patients than hyperbaric oxygen therapy. The mechanism of this combination therapy may be related to the improvement in immunity-related cytokine levels.Keywords: Glucocorticoid, Hyperbaric oxygen, Delayed encephalopathy after carbon monoxide poisoning, Efficacy, Immunit