Air pollution significantly increases morbidity and mortality due to endothelial dysfunction, but the mechanism of this process is unclear. Particulate matter (PM) is one of the important components in air pollution that can cause endothelial vascular dysfunction through exacerbation of atherosclerosis and inflammation of the respiratory system. The evidence shows that air pollution contributes to the incidence of acute cardiovascular disease that begins with the occurrence of vascular endothelial dysfunction through various pathways, including systemic inflammation, activity of homeostatic pathways, accelerated atherosclerosis, plaque instability, changes in autonomic control, and cardiac arrhythmias and direct inhalation, causes vasoconstriction, hypertension, and platelet aggregation.
PM can cause oxidative stress through the direct formation of reactive oxygen species (ROS) through the physico-chemical properties of the surface of the particulate material. One mechanism that is thought to play a role is the occurrence of oxidative stress which will then increase ROS in the body, namely hydrogen peroxide (H2O2) and hydroxyl radicals (–OH). Free radicals, especially hydroxyl radicals (–OH), can cause cell damage through the so-called lipid peroxidation, with the final result in the form of compounds that are damaging to cells, one of which is malondialdehyde (MDA). Increased levels of MDA in blood plasma can be an indicator of oxidative stress. This oxidative stress then induces cell degeneration and causes endothelial cell dysfunction (Lin et al., 2015; Kozlov et al., 2016).
The antioxidant enzyme SOD acts as a front-line protective enzyme against superoxide anion, catalyzing superoxide to hydrogen peroxide and oxygen. The O2 molecule will be reduced to H2O with the addition of 4 electrons, forming If the number of electrons that reduce the molecule is less than 4, then the phosphorylation process is imperfect, so free radicals formed from soot can move into the blood vessels. When soot particulates enter the body, the body will carry out a defense mechanism in the form of increased production of proinflammatory cytokines by inflammatory cells, especially macrophages. Macrophages can secrete proinflammatory cytokines. These cytokines activate nuclear factor kappa B (NFкB) in cells that respond to inflammation. Activation of NF-кB will trigger the release of proinflammatory cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrotic factor-α (TNF-α) (Erta et al., 2012; Salomon et al., 2018; Lewis and Elks, 2019; Nabarawy et al., 2019; Silva et al., 2019). These cytokines will stimulate immune cells and vascular endothelial cells to release inflammatory cytokines. Excessive production of inflammatory cytokines and ROS will result in tissue damage, which can lead to impaired vascular cell dysfunction.
Curcuma longa or turmeric (turmeric) is a plant that is a genus of the family Zingiberaceae. Curcuma longa, also known as turmeric, is one of the native herbs/ spice plants from Southeast Asia, spread from India, Malaysia, and Indonesia. Many studies report the polyphenol content of curcumin in C. longa and its pharmacological effects, including as an antioxidant, anti-inflammatory, anti-microbial, and anti-cancer alternative (Raju et al., 2006; Sadeghi et al., 2018; Song et al., 2019).
This study aims to prove that the administration of C. longa can reduce MDA, TNF-α, and IL-6 levels in Rattus norvegicus exposed to soot particulates. Based on these facts, researchers are encouraged to carry out further research on the mechanism of exposure to air pollutant particles, especially vascular dysfunction and the effect of Curcuma Longa as an anti-inflammatory and antioxidant using laboratory experimental methods and mice as experimental animals.
This study aims to prove the effectiveness of turmeric extract on mice ( Rattus novergicus ) exposed to soot on Ox-LDL and eNOS levels. The subjects of this study were 30 male mice which were divided into 5 treatment groups with the following: (C-): negative control (without exposure to soot particulates and without treatment; (C+): positive control (mice exposed to particulate soot at a concentration of 1,064 mg/m3;) (T1): Treatment group 2, mice exposed to particulate soot at a concentration of 1,064 mg/m3 for 8 hours and given C. longa at a dose of 1 mg/kg body weight; (T2): Treatment group 3 was mice exposed to soot particulates at a concentration of 1,064 mg/m3 for 8 hours and given C. longa at a dose of 2 mg/kg body weight; (T3): Treatment group 4 was mice exposed to soot particulates at a concentration of 1,064 mg/m3 for 8 hours and given C. longa at a dose of 3 mg/kg body weight. The research was conducted for 30 days. The T3 group had lower ox-LDL and eNOS levels than the C+ group, and the difference was significant (p>0.05). It can be concluded that giving turmeric extract at a dose of 3 mg/kg BW to rats ( Rattus novergicus ) exposed to soot at a concentration of 1064 mg/m3 for 8 hours reduced ox-LDL levels while increasing eNOS level.
Author: Widjiati
Details of this study can be viewed in our article at
Open Veterinary Journal, (2023), Vol. 13(1): 11–19
Article link:
https://www.openveterinaryjournal.com/fulltext/100-1660403353.pdf?1677450961
