The Amomum tsao-ko Essential Oils Inhibited Inflammation and Apoptosis through p38/JNK MAPK Signaling Pathway and Alleviated Gentamicin-Induced Acute Kidney Injury

Abstract

The clinical application of gentamicin may lead to acute kidney injury (AKI), and the nephrotoxicity of gentamicin is related to the pathological mechanism of several oxidative and inflammatory cytokines. Plant-derived essential oils have good anti-inflammatory and antioxidant properties. This study aimed to clarify the protective effect of Amomum tsao-ko essential oils (AOs) on gentamicin-induced AKI in rats and its possible mechanism. The rat AKI model was induced by intraperitoneal injection of gentamicin. After 14 days of oral AO treatment, the renal function and pathological changes of the kidney tissues were evaluated, and the level of kidney tissue oxidative stress was detected. The content of inflammatory cytokines was measured by ELISA. The expression of ERK1/2, JNK1/2, p38, NF-κB, caspase-3, and Bax/Bcl-2 proteins were estimated by Western blot analysis. The results showed that taking AO reduced the contents of serum urea and creatinine in AKI rats and improve the pathological changes and oxidative stress of the kidney tissue in rats. At the same time, AO reduced inflammation and apoptosis during AKI by regulating the MAPK pathway. The data show that AO has a protective effect on the kidneys and may be a potential drug for treating kidney injury.

Keywords: Amomum tsao-ko; MAPK; acute kidney injury; essential oils; gentamicin.

Figure 1

TIC diagram of Amomum tsao-ko essential oils.

Figure 2

Effect of AO on histopathological changes of kidneys in GM-treated rats. Representative micrographs of each experimental group stained with hematoxylin and eosin and TUNEL, magnification ×200.

Figure 3

Effects of AO on kidney function indexes in AKI rats. (a) Serum creatinine, (b) blood urea nitrogen, and (c) urinary protein were measured on the first day after the last administration. The data are expressed as means ± standard deviation; compared with the model group, ** p < 0.01; compared with the control group, ## p < 0.01 (n = 6).

Figure 4

Regulation of AO on markers of oxidative tissue damage in kidney tissue of AKI rats. (a) Glutathione peroxidase (GSH-Ps), (b) malondialdehyde (MDA), (c) superoxide dismutase (SOD), (d) nitric oxide synthase (NOS), (e) nitric oxide (NO); # p < 0.05 vs. control group, ## p < 0.01 vs. control group. * p < 0.05,** p < 0.01 vs. model group (n = 6).

Figure 5

Effect of AO on the level of serum inflammatory factors in GM-treated rats. (a) IL-6 (interleukin 6), (b) IL-1β (interleukin -1β), and (c) TNF-α (tumor necrosis factor-α); n = 6; ## p < 0.01 vs. control group. ** p < 0.01 vs. model group.

Figure 6

Effect of AO on the expression of MAPK pathway-related proteins in GM-induced AKI kidney of rats. ## p < 0.01 vs. control group. * p < 0.05, ** p < 0.01 vs. Model group.

Figure 7

Effect of AO on the expression of proteins related to apoptosis and inflammation in kidneys of AKI rats induced by GM. ## p < 0.01 vs. control group. * p < 0.05 ,** p < 0.01 vs. model group.

Figure 8

How AO affects the speculative mechanism of AKI caused by GM.