Kyle J. Norton
Inflammation is the natural response of the immune system macrophages, the first line of defense in stimulating the production of inflammatory cytokines to protect our body against the infection caused by foreign microorganisms during the acute phase of body damage and injury.
Truly, the main focus of inflammation is to repair damage and injury.
Most cases of infection associated with inflammation are stopped at the acute phase. The wound or injury is slowly recovered.
Acute inflammation occurs quickly or within hours and lasts a few days or weeks and the damaged tissues are healed themselves after all pathogens are killed off.
However, if the immune system can not completely eradicate all invaders in the acute phase of infection, it will compromise, leading to chronic low-grade inflammation, a major cause of cardiovascular disease, arthritis, and diabetes.
Chronic inflammation is a low-grade inflammation caused by the inability of the immune system to eliminate the invasive pathogens that occurred in the acute phase of infection.
Any inflammation that lasts more than 8 weeks is considered chronic inflammation.
Believe it or not, worldwide, 3 of 5 death are results from chronic inflammatory diseases like stroke, chronic respiratory diseases, heart disorders, cancer, obesity, and diabetes.
In the US, chronic inflammatory diseases affect more than 50 million Americans each year.
Anti-inflammation is a process that inhibits the pro-inflammatory cytokines without affecting the immune system's activity against pathogens.
Diseases associated with low-grade inflammation include diabetes and cardiovascular.
Conventionally, Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most common medical drugs such as aspirin. ibuprofen in reducing inflammation associated with pain-relieving.
Oleanolic acid is a phytochemical in the subclass of Triterpenoid, belonging to the group of Terpenes found abundantly in honey mesquite, garlic, java apple, clove, etc.
In finding a potential plant in the prevention and treatment of chronic diseases, researchers examined the effect of Oleanolic acid (OA), as a triterpenoid, has anti-oxidant, anti-inflammatory, and anti-apoptotic activities on motor function in Spinal cord injury (SCI) mice.
According to the results of the analysis,
* OA in a dose-dependent manner up-regulated the spinal cords of SCI mice and improved the blood-spinal cord barrier.
* OA treatments significantly reduced apoptotic cell death in spinal cord samples of SCI mice by decreasing the expression of pro-apoptotic cleaved Caspase-3.
* Furthermore, OA significantly attenuated the pro-inflammatory response in SCI mice.
* Most importantly, SCI mice exhibited higher activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) signaling pathways involved in cell death but these effects were clearly blocked in SCI mice with OA treatments.
In other words, in vivo, OA exerted protective effects against SCI induced by lipopolysaccharide (LPS)-stimulated mouse neurons mainly through the suppression of apoptosis and inflammatory response.
Taken altogether, Oleanolic acid may be considered a remedy that processes inflammatory and apoptotic activity, pending the confirmation of the larger sample size and multicenter human study.
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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the Karate GB Daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as the international journal Pharma and Bioscience, ISSN 0975-6299.
Sources
(1) Oleanolic acid inhibits mouse spinal cord injury through suppressing inflammation and apoptosis via the blockage of p38 and JNK MAPKs by Wang JL1, Ren CH1, Feng J2, Ou CH3, Liu L4. (PubMed)
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