Abstract
Background Epidemiological studies have shown that exposure to PM induces oxidative stress, leading to a variety of health problems. In particular, PM2.5 contains a lot of substances harmful to the human body and penetrates into the lungs to induce lung injury. At the same time, there is increasing evidence that oxidative stress also affects the severity of lung injury. However, there is still no good way to reduce or eliminate these hazards. In the future, more experimental research is needed to further confirm the mechanisms of these hazards and formulate effective preventive measures and treatment plans for their hazard mechanisms. Curcumin has been reported to reduce oxidative stress and inflammatory damage and protect organs. Objective To investigate whether curcumin can play a protective role against PM2.5-induced oxidative stress and inflammatory damage by inducing expression of the HO-1/CO/P38 MAPK pathway. Methods In this experiment, PM2.5 was dropped into the trachea to establish a lung injury model in mice. 28 SPF-grade male Kunming mice were randomly divided into 4 groups: normal control group, saline control group, PM2.5 treatment group, and curcumin intervention group. Albumin (ALB), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) were measured in alveolar lavage fluid (BALF) to assess lung tissue damage. Colorimetric detection of oxidative stress indicators such as MDA, GSH-PX, T-AOC, and CAT in the lung tissue was performed. The levels of IL-6 and TNF-α in the lung tissue were determined by ELISA. Histopathological examination was used for the assessment of alveolar epithelial damage. The protein expression of the HO-1/P38 MAPK pathway in the lung tissue was determined by Western blot and immunohistochemistry. Endogenous CO was detected by spectrophotometry. The results showed that the expression of the HO-1/CO/P38 MAPK protein in the lung tissue was significantly increased in the curcumin intervention group compared with the PM2.5 treatment group, and it was statistically significant (P < 0.05). Compared with the PM2.5 treatment group, the curcumin intervention group can reduce the amount of ALB, LDH, and ALP in BALF; reduce the levels of MDA, IL-1, and TNF-α in the lung tissue; and improve GSH-PX, T-AOC, and CAT levels, but there is no statistical difference (P > 0.05). Conclusion We found that PM2.5 can cause lung damage through oxidative stress and inflammatory responses. Oxidative stress and inflammatory responses increase the expression of HO-1/CO/P38 MAPK. The intervention of curcumin can further increase the expression of HO-1/CO/P38 MAPK.
Highlights
Epidemiological studies have shown that exposure to PM induces oxidative stress, leading to a variety of health problems
The results showed that the expression of the Heme oxygenase 1 (HO-1)/carbon monoxide (CO)/P38 MAPK protein in the lung tissue was significantly increased in the curcumin intervention group compared with the PM2.5 treatment group, and it was statistically significant (P < 0 05)
In the inhaled PM2.5, it usually contains metals such as iron, copper, and zinc [33, 34]; on the one hand, the redox-active metal in PM2.5 initiates a series of cleavage reactions and the formation of free radicals, which can lead to cell membrane lipids, peroxidation, and inflammation [32]; on the other hand, PM2.5 is phagocytized by alveolar macrophages, releasing airway inflammatory mediators, mainly IL-6, IL-8, IL-13, Tumor necrosis factor- (TNF-)α, macrophage inflammatory protein-1, granulocytemacrophage colony-stimulating factors, etc. [35, 36]
Summary
Air pollution poses a huge environmental risk to health. According to the Global Burden of Disease report, outdoor fine particulate matter (PM2.5) exposure is the fifth largest risk factor for death in the world, resulting in 4.2 million deaths and more than 100 million disability-adjusted lifeyear losses. After exposure to PM2.5, it can promote the release of various inflammatory factors in the lungs, produce a large number of oxygen free radicals, destroy the body’s oxidation/antioxidant balance, and cause damage to the respiratory system and other systems. HO-1 exerts physiological functions such as antioxidation, anti-inflammation, and antiapoptosis through these effector molecules in vivo; bilirubin is an effective antioxidant in vivo, which has the function of scavenging free radicals, and participates in maintaining the balance of oxidation and antioxidant mechanisms in vivo. Many studies have shown that [22,23,24,25] curcumin has obvious biological effects such as antioxidative stress, anti-inflammation, and antiapoptosis and plays a role in multiple molecular targets of multiple pathways, protecting multiple organ functions. An early intervention method of curcumin was used to establish a mouse lung injury model based on PM2.5-induced lung injury-related experiments [28], to investigate whether curcumin can alleviate lung injury through the HO-1/CO/P38 MAPK pathway
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
