Study on the Mechanism of Curcumin Regulating Lung Injury Induced by Outdoor Fine Particulate Matter (PM2.5)

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.

The Protective Effects of Shengmai Formula Against Myocardial Injury Induced by Ultrafine Particulate Matter Exposure and Myocardial Ischemia are Mediated by the PI3K/AKT/p38 MAPK/Nrf2 Pathway

“…Meanwhile, in our in vitro study, elevated levels of ROS were observed in the H9C2 cells exposed to UFPM, consistent with an imbalance in the oxidation/reduction observed in our in vivo study. A previous study demonstrated a significant difference in the expression levels of MDA, CAT, and GSH-Px in lung tissues of PM2.5-treated mice compared with saline-treated control mice ( Huang et al, 2019 ). Similar increases in the levels of HO-1 and NOX in the lung and heart have been reported after particle exposure in rats; the differences were dependent on particulate size ( Aztatzi-Aguilar et al, 2015 ).…”

Assessment of particulate matter toxicity and physicochemistry at the Claim 28 uranium mine site in Blue Gap, AZ

“…Another recent study was done by Huang et al 2019, where traffic-based PM2.5 was instilled into mouse trachea as a PM2.5-induced injury. In this paper, the authors found lung injury to be the result of oxidative damage and induction of inflammatory processes (Huang et al, 2019). These are just a few current studies, but PM2.5 continues to be a popular area of environmental research.…”

MicroRNA-760 Resists Ambient PM2.5-induced Lung Injury Through Upregulating Heme-oxygenase 1 Expression

“…Unlike PM 10 , PM 2.5 is su ciently small in size to reach the alveoli of the lungs, thus exhibits a signi cant impact on human health [1][2][3][4]. According to the Global Burden of Disease report, airborne PM 2.5 exposure might contribute to 4.2 million deaths and 100 million disability-adjusted life-year losses, and serves as the fth largest risk factor for death in the world [5]. Epidemiological studies have consistently shown that long-term exposure to high levels of PM 2.5 is associated with high risks of ischemic heart disease, stroke, lung cancer, and chronic obstructive pulmonary disease [6,7].…”

“…Numerous evidences suggested that oxidative stress and in ammation play a critical role in PM 2.5 induced lung injury [5,[8][9][10]. Exposure to PM 2.5 has been reported to stimulate the release of various proin ammatory molecules in the lung.…”

“…In most tissues/organs, except for the spleen, HMOX1 is usually expressed at low levels; however, it is highly inducible in response to a variety of stimuli to protect cells against oxidative and in ammatory injury. Several lines of evidence have indicated that PM 2.5 -induced oxidative stress might function as a signaling molecule to activate HMOX1 expression [5,13,17,18] ; however, the detailed mechanism remains unrevealed.…”