Abstract
In this study, we found that chloroform fraction (CF) from TJP ethanolic extract inhibited lipopolysaccharide (LPS)-induced production of nitric oxide (NO) and intracellular ROS in RAW264.7 cells. In addition, expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) genes was reduced, as evidenced by western blot. Our results indicate that CF exerts anti-inflammatory effects by down-regulating expression of iNOS and COX-2 genes through inhibition of MAPK (ERK, JNK and p38) and NF-κB signaling. Similarly we also evaluated the effects of CF on LPS-induced acute lung injury. Male Balb/c mice were pretreated with dexamethasone or CF 1 h before intranasal instillation of LPS. Eight hours after LPS administration, the inflammatory cells in the bronchoalveolar lavage fluid (BALF) were determined. The results indicated that CF inhibited LPS-induced TNF-α and IL-6 production in a dose dependent manner. It was also observed that CF attenuated LPS-induced lung histopathologic changes. In conclusion, these data demonstrate that the protective effect of CF on LPS-induced acute lung injury (ALI) in mice might relate to the suppression of excessive inflammatory responses in lung tissue. Thus, it can be suggested that CF might be a potential therapeutic agent for ALI.
Highlights
Inflammation is a complex biological response to protect against a wide range of injuries caused by infectious agents, antigen challenge, and physical, chemical or traumatic damage [1]
IκB-α phosphorylation and degradation, and further nuclear, the translocation of p65, which in turn. These results indicated that the molecular mechanism for the chloroform fraction (CF)-mediated attenuation of LPS-induced leads to the suppression of inflammatory mediators
nitric oxide (NO) can mediate the functions of many types of cells at the LPS-stimulation of macrophages disrupts the balance of the intracellular reduction-oxidation site of inflammation, including T lymphocytes, macrophages, synovial fibroblasts, osteoclasts, and state, which leads to [19]
Summary
Inflammation is a complex biological response to protect against a wide range of injuries caused by infectious agents, antigen challenge, and physical, chemical or traumatic damage [1]. De-regulation and perpetual activation of inflammation can lead to many diseases, such as rheumatoid arthritis, chronic asthma, multiple sclerosis, inflammatory bowel disease and psoriasis [2]. One of the most potent stimuli to macrophages is the bacterial endotoxin lipopolysaccharide (LPS), which induces the production of a variety of cytokines and inflammatory mediators including nitric oxide (NO), prostaglandin E2. Trapa japonica has been used as ethno-medicine for the treatment of gastric ulcer, diarrhea, hangover after alcohol consumption, and dysentery. Various other pharmacological activities of Trapa japonica include, antioxidant activity, hepatoprotective activity, and antidiabetic activity [5,6]. Trapa japonica has long been used in folk medicine, little has been explored about the physiological functions of its active ingredients
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