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Lymphstasis, Inflammation and Atherogenesis – Connecting the Dots
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
The standard therapy is to treat acute inflammation with anti-inflammatories, like ibuprofen and Aleve. These Cox 2 inhibitors block the “pro-inflammatory” arachidonic acid and prostaglandin 2 series, which are also necessary to create several of the SPM substances.
Cancer
Published in Sally Robinson, Priorities for Health Promotion and Public Health, 2021
Like atherosclerosis and cardiovascular disease, obesity and type 2 diabetes, cancer is often described as a chronic low-grade inflammatory disease. Acute inflammation occurs when we sustain an injury. Blood vessels dilate, blood flow increases and white blood cells cluster around the wound to alert cytokines, activate the immune system and support healing. If the body exhibits persistent inflammation at a low level and ‘doesn’t switch off’, it causes damage and disease. Low-grade inflammation may be triggered by internal and external threats, and these include age, excess body fat, a diet rich in saturated fat, trans fat and sugar, tobacco smoking and stress (Pahwa et al., 2020). The causes of cancer can be divided into the non-modifiable risk factors that we can’t change, and the modifiable ones that we can. Many may initially prompt low-grade inflammation which, in turn, may encourage cancer.
AI and Chronic Inflammation
Published in Louis J. Catania, AI for Immunology, 2021
Standard treatments used for acute inflammation (steroids, NSAIDs discussed in Section “Acute Inflammation”, Chapter 2, Page 22) are of some value in chronic inflammation, but rarely prove adequate for maximal therapy (although the corticosteroid dexamethasone is proving to be of some value in COVID-19 – more in Chapter 5). Rather, the principal approach in treating chronic inflammation is obviously to suppress those immunochemical and molecular biologic processes (right side of Figure 2.3) that are promoting inflammatory (pro-inflammatory cytokine) changes and conversely, to stimulate and promote those agents that inhibit the inflammatory process (see Tables 3.1 and 3.2). In some cases, drugs are used for these dual purposes and sometimes the actual cells and chemicals (humoral agents) involved in a bodily process are used to supplement the body’s own defense mechanisms. As an example, monoclonal antibodies (any drug with the name suffix, “…mab”) are laboratory-engineered antibodies used to mimic the immune system’s own antibodies for a specific antigen and its resultant chronic inflammation (see also Chapter 5, page 106).
Pentapeptide modified ethosomes for enhanced skin retention and topical efficacy activity of indomethacin
Published in Drug Delivery, 2022
Jiangxiu Niu, Ming Yuan, Hongying Li, Yao Liu, Liye Wang, Yanli Fan, Yansong Zhang, Xianghui Liu, Lingmei Li, Jingxiao Zhang, Chenyu Zhao
The anti-inflammatory activity of developed formulations was investigated in the acute inflammation method (Gao et al., 2020; Niu et al., 2020). Dimethylbenzene (20 μL per side) was topically applied to both sides of the right ear after 60 min of transdermal administration with the formulation. The left ear remained untreated. The mice were sacrificed by cervical dislocation after being treated with dimethyl benzene for 30 min. The right ear and left ear were cut off at the same position with a stainless steel punch with a diameter of 8 mm and weighed. The ear edema and the inhibitory ratio of ear edema were calculated by the following equation: Ear edema = weight of the right (treated) ear – weight of the left (untreated) ear Inhibitory ratio of ear edema = [(mean of normal control edema – mean of treatment group edema)/mean of normal control edema] × 100%.
Structure-guided approach on the role of substitution on amide-linked bipyrazoles and its effect on their anti-inflammatory activity
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Souraya A. Domiati, Khaled H. Abd El Galil, Mohammed A. S. Abourehab, Tamer M. Ibrahim, Hanan M. Ragab
Acute inflammation is rapid in onset and of a few hours’ duration. It is characterised by four cardinal signs: hotness, redness, swelling, and pain. Those develop experimentally by the subcutaneous administration of Formalin. Immediately, edoema, hyperalgesia, and erythema develop due to the migration of neutrophils to the site and the generation of pro-inflammatory agents such as bradykinin, histamine, tachykinins, reactive oxygen, and nitrogen species. Thus, edoema is quantified by measuring the increase in paw size, which is maximal around 4 h post formalin injection48. Accordingly, in the current study, edoema inhibition was recorded after 30 min and 4 h of edoema induction. Results (Figure 6) showed higher percentages of inhibition after 30 min for compound 5a as compared with the positive control indomethacin, and a similar inhibition for 5c and 5e to the positive control celecoxib. At 4 h, compounds 5a and 5c showed a higher inhibition than both indomethacin and celecoxib. Overall, these results reflect promising in vivo anti-inflammatory performance for most of these compounds.
Upregulation of claudin‑4 by Chinese traditional medicine Shenfu attenuates lung tissue damage by acute lung injury aggravated by acute gastrointestinal injury
Published in Pharmaceutical Biology, 2022
Yueliang Zheng, Mian Zheng, Jing Shao, Chengxing Jiang, Jian Shen, Rujia Tao, Yuqin Deng, Yingge Xu, Yuanqiang Lu
Acute lung injury (ALI) is a common clinical syndrome of an acute systemic inflammatory process in the lung that disrupts endothelial and epithelial barriers (Rubenfeld et al. 2005; Johnson and Matthay 2010; Schmidt and Tuder 2010). ALI and its most severe form, acute respiratory distress syndrome (ARDS), are the major causes of morbidity and mortality in critical patients. The incidence of ALI is about 17–34 annual cases per 100,000 people, with mortality rates of 34–58% (MacCallum and Evans 2005). Common causes of ALI/ARDS are sepsis, trauma, shock, aspiration, inhalation injury, multiple blood transfusion, acute pancreatitis, and even certain drug toxicities. Direct or systemic lung injury might initiate the disease process, while the related inflammatory response propagates lung injury, especially when the disease is coupled with other insults related to the lung. In the early stage of ALI, accumulated tissue damage of the endothelial and epithelial barriers increases lung permeability, which causes alveolar edoema (Matthay et al. 2000). Then, inflammatory responses characterized by secretion of inflammatory cytokines [e.g., tumour necrosis factor alpha (TNF-α), interleukin (IL)-6, and IL-1β] and influx of neutrophils to the alveolar space are activated (Ward 2003). This acute inflammation enhances tissue damage, which in turn aggravates the disease. Meanwhile, fibroproliferation occurs in the alveolar hyaline membranes, as well as varying degrees of interstitial fibrosis.