Rabbit Anti-Human TNF Polyclonal Antibody

Inflammation is an essential biological process for maintaining homeostasis in the body. However, excessive inflammatory response is closely related to many chronic diseases. Ammonia is a known environmental pollutant and a main harmful gas in the environment of livestock house. It causes deterioration of air quality and poses a threat to human and animal health. Chickens are very sensitive to ammonia. In order to assess the toxicity of ammonia to the heart, the pathology, ATPase activities, markers of oxidative stress, inflammatory pathways and inflammation markers were investigated in the hearts of chickens exposed to ammonia. The results showed that the cardiac pathological structure, oxidative stress index, and ATPase activity changed significantly in ammonia-treated chickens. In addition, the inflammation pathways (JAK/STAT and MAPK) were activated in the ammonia group, and the inflammatory markers (COX-2, TNF-alpha, NF-kappa B and PPAR-gamma) were significantly altered at both mRNA and protein levels. In conclusion, excess ammonia can activate inflammatory pathways through oxidative stress and abnormal energy metabolism, and induce cardiac inflammatory injury. Our findings will provide a new insight for better assessing the toxicity mechanism of ammonia on the heart. (C) 2020 Elsevier B.V. All rights reserved.

Background: Combination drug therapy has become an effective strategy for inflammation control. The anti-inflammatory capacities of silibinin and thymol have each been investigated on its own, but little is known about the synergistic anti-inflammatory effects of these two compounds. Purpose: This study aims to investigate the synergistic anti-inflammatory effects of silibinin and thymol when administered in combination to lipopolysaccharide (LPS)-induced RAW264.7 cells. Methods: RAW264.7 cells were pre-treated with silibinin and thymol individually or in combination for 2 h before LPS stimulation. Cell viability was detected by the MTT assay. Nitric oxide (NO) production was measured by Griess reagent. Reactive oxygen species (ROS) was evaluated by 2',7'-dichlorofluorescein-diacetate. ELISA was used to detect tumour necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6). Western blot was performed to analyse the protein expression of LPS-induced RAW264.7 cells. Results: We observed a synergistic anti-inflammatory effect of silibinin and thymol when administered in combination to LPS-induced RAW264.7 cells. Silibinin combined with thymol (40 mu M and 120 mu M respectively, with the molar ratio 1:3) had more potent effects on the inhibition of NO, TNF-alpha, and IL-6 than those exerted by individual administration of these compounds in LPS-induced RAW264.7 cells. The combination of silibinin and thymol (40 mu M and 120 mu M respectively, with the molar ratio 1:3) strongly inhibited ROS and cyclooxygenase-2 (COX-2). More importantly, the combination of silibinin and thymol (40 mu M and 120 mu M respectively, with the molar ratio 1:3) was also successful in inhibiting nuclear factor-kappa B (NF-kappa B) and mitogen-activated protein kinase (MAPK) activities. Our results suggest that the synergistic anti-inflammatory effects of silibinin with thymol were associated with the inhibition of NF-kappa B and MAPK signalling pathways. Conclusion: The combination of silibinin and thymol (40 mu M and 120 mu M, respectively, with the molar ratio 1:3) could inhibit inflammation by suppressing NF-kappa B and MAPK signalling pathways in LPS-induced RAW264.7 cells.