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. 2018 Jul 29:2018:9098627.
doi: 10.1155/2018/9098627. eCollection 2018.

The Kidney Injury Induced by Short-Term PM2.5 Exposure and the Prophylactic Treatment of Essential Oils in BALB/c Mice

Yining Zhang  1 , Qiujuan Li  2 , Mengxiong Fang  1 , Yanmin Ma  1 , Na Liu  1 , Xiaomei Yan  1 , Jie Zhou  3 , Fasheng Li  1
Affiliations

The Kidney Injury Induced by Short-Term PM2.5 Exposure and the Prophylactic Treatment of Essential Oils in BALB/c Mice

Yining Zhang et al. Oxid Med Cell Longev. .

Abstract

PM2.5 is well known as a major environmental pollutant; it has been proved to be associated with kidney diseases. The kidney damage involves oxidative stress and/or inflammatory response. NOX4 is a major source of reactive oxygen species (ROS) generation in the kidney, and the excessive generation of ROS is recognized to be responsible for oxidative stress. To elucidate whether short-term PM2.5 exposure could induce kidney damage, we exposed BALB/c mice to PM2.5 intratracheally and measured the biomarkers of kidney injury (KIM-1, cystatin C), oxidative stress (MDA, SOD-1, and HO-1), and inflammatory response (NF-κB, TNF-α). Acute kidney damage and excessive oxidative stress as well as transient inflammatory response were observed after PM2.5 installation. The overexpression of some components of the angiotensin system (RAS) after PM2.5 exposure illustrated that RAS may be involved in PM2.5-induced acute kidney injury. CEOs (compound essential oils) have been widely used because of their antioxidant and anti-inflammation properties. Treatment with CEOs substantially attenuated PM2.5-induced acute kidney injury. The suppression of RAS activation was significant and earlier than the decrease of oxidative stress and inflammatory response after CEOs treatment. We hypothesized that CEOs could attenuate the acute kidney injury by suppressing the RAS activation and subsequently inhibit the oxidative stress and inflammatory response.

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Figures

Figure 1
Figure 1
Mouse kidney injury after administration by PM2.5 or saline (bar = 50 μm). Samples were stained using H&E, no significant pathological change in the PM2.5 group compared with the control group (a). KIM-1 mRNA was assayed by RT-PCR, serum UA and cystatin C were assessed using chemiluminescence. KIM-1 mRNA expression of kidney tissues (b) and serum UA (c) and serum cystatin C (d) increased after exposure (n = 6, ∗∗P < 0.01 and ∗P < 0.05 versus the control group).
Figure 2
Figure 2
PM2.5 induced oxidative stress and inflammatory response. PM2.5 increased MDA (a) and H2O2 (b) level (n = 6). The mRNA expression of HO-1 (e), NOX-4 (f), NF-κB (g), and TNF-α (h) was promoted and SOD-1 (d) as well as GSH-PX (c) was suppressed by PM2.5 (n = 6). The protein generation of NOX4 (i), NF-Κb (j), and TNF-α (k) was in accordance with their gene levels (n = 4). ∗∗P < 0.01 and ∗P < 0.05 versus the control group.
Figure 3
Figure 3
PM2.5 activated the RAS. An augment in the angiotensin-converter enzyme (ACE) (a) and angiotensin-receptor type-I (AT1R) (b) after PM2.5 exposure (n = 4, ∗∗P < 0.01 and ∗P < 0.05 versus the control group).
Figure 4
Figure 4
CEOs alleviated acute kidney injury. KIM-1 mRNA expression in kidney tissues (a), serum UA (b), and serum cystatin C (c) decreased after administration of CEOs (n = 6, ∗∗P < 0.01 and ∗P < 0.05 versus the PM2.5 + saline group).
Figure 5
Figure 5
CEOs decreased oxidative stress and inflammatory response. MDA level (a), H2O2 level (b), and the mRNA expression of HO-1 (e), NOX-4 (f), NF-κB (g), and TNF-α (h) were suppressed; SOD-1 mRNA expression (d) and the level of GSH-PX (c) were increased (n = 6). The protein level of NOX-4 (i), NF-κB (j), and TNF-α (k) decreased after the treatment of CEOs (n = 4) (∗∗P < 0.01 and ∗P < 0.05 versus the PM2.5 + saline group).
Figure 6
Figure 6
CEOs suppressed the RAS. ACE (a) and AGTR1 (b) were downregulated in the early stage (n = 4, ∗∗P < 0.01 and ∗P < 0.05 versus the PM2.5 + saline group).
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