TY - JOUR
T1 - The effect of soot particulate towards vascular cell adhesion molecule-1 (Vcam-1) expression in the mechanism of cardiovascular system disruption
AU - Leonard, Edmond
AU - Aminuddin, Muhammad
N1 - Publisher Copyright:
© 2020, World Informations Syndicate. All rights reserved.
PY - 2020/4/1
Y1 - 2020/4/1
N2 - Background: Air pollution is associated with cardiovascular morbidity and mortality; however, the underlying mechanisms are not yet clearly understood. Several previous studies have implicated potential mechanism action including oxidative stress, systemic inflammation, autonomic dysfunction, and endothelial dysfunction. Several epidemiological studies have examined the association between ICAM-1, VCAM-1 and particulate matter. Objective: To describe the effect of soot particulate exposure in VCAM-1 expression in the mechanism of cardiovascular dysfunctions. Method: The experiment was conducted in laboratory female rats (Rattus novergicus) and consisted of 3 groups: Control group (n=10), without soot particulate exposure; Treatment 1 group (n=12), exposed by soot particulate with the concentration of 532 mg/m3 an hour each day for 30 days; Treatment 2 group (n=12), exposed by soot particulate with the concentration of 1064 mg/m3 an hour each day for 30 days.The expression of VCAM-1 on cardiac tissue was measured after the end of treatment by immunohistochemical examination. The differentiation of VCAM-1 expression among the groups was tested using the Kruskal-Wallis test and the Mann-Whitney test. Results: The mean rank of VCAM-1 expression in the control group, treatment group 1 and treatment group 2 was significantly different (8.85, 17.63, 24.58, p=0.001). There was a significant difference in VCAM-1 expression by using the Mann-Whitney test among groups (p <0.05). Conclusion: The exposure to soot particles increased VCAM-1 expression significantly in laboratory animals. Our findings indicated the important role of the inflammatory activation pathway as a response to soot particulate exposure in the mechanism of cardiovascular disease.
AB - Background: Air pollution is associated with cardiovascular morbidity and mortality; however, the underlying mechanisms are not yet clearly understood. Several previous studies have implicated potential mechanism action including oxidative stress, systemic inflammation, autonomic dysfunction, and endothelial dysfunction. Several epidemiological studies have examined the association between ICAM-1, VCAM-1 and particulate matter. Objective: To describe the effect of soot particulate exposure in VCAM-1 expression in the mechanism of cardiovascular dysfunctions. Method: The experiment was conducted in laboratory female rats (Rattus novergicus) and consisted of 3 groups: Control group (n=10), without soot particulate exposure; Treatment 1 group (n=12), exposed by soot particulate with the concentration of 532 mg/m3 an hour each day for 30 days; Treatment 2 group (n=12), exposed by soot particulate with the concentration of 1064 mg/m3 an hour each day for 30 days.The expression of VCAM-1 on cardiac tissue was measured after the end of treatment by immunohistochemical examination. The differentiation of VCAM-1 expression among the groups was tested using the Kruskal-Wallis test and the Mann-Whitney test. Results: The mean rank of VCAM-1 expression in the control group, treatment group 1 and treatment group 2 was significantly different (8.85, 17.63, 24.58, p=0.001). There was a significant difference in VCAM-1 expression by using the Mann-Whitney test among groups (p <0.05). Conclusion: The exposure to soot particles increased VCAM-1 expression significantly in laboratory animals. Our findings indicated the important role of the inflammatory activation pathway as a response to soot particulate exposure in the mechanism of cardiovascular disease.
KW - Soot particulate
KW - Vascular cell adhesion molecule-1 (VCAM-1)
UR - http://www.scopus.com/inward/record.url?scp=85088233535&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:85088233535
SN - 0971-720X
VL - 20
SP - 830
EP - 835
JO - Medico-Legal Update
JF - Medico-Legal Update
IS - 2
ER -