Chenopodium botrys Extract Affects Acute Kidney Injury Caused by Rhabdomyolysis in Rats Through TNF/NF-κB Signaling Pathway

Abstract

Due to the anti-inflammatory and antioxidant properties of the Chenopodium botrys and the pathological mechanisms of rhabdomyolysis in the kidney, this plant can be used to improve the symptoms of this disease. Then, in this study, we investigated the effects of this herb in improving kidney injury by rhabdomyolysis. Animals were divided into five groups: control, glycerol (received it for rhabdomyolysis induction), extract (received 12 mg/kg C. botrys extract), and treatment groups with dexamethasone (0.03 mg/kg) and extract (12 mg/kg). The extract was analyzed using HNMR. After a week, blood and urine samples were taken to measure protein, urea, and creatinine. Then, the animals were sacrificed, and the kidney tissue was removed to examine the antioxidant, TNF-α, and histopathological evaluations. Also, NF-κB gene expression was investigated. The serum creatinine, TNF-α, and NF-κB ratio significantly increased and antioxidant capacity decreased in the glycerol group compared with the control. Pathological evaluation also showed severe renal damage based on the related criteria. In the treatment groups with dexamethasone and especially extract, the considered parameters attenuated relatively compared with the glycerol group. Kidney damage and functional impairment associated with rhabdomyolysis, as well as the inflammatory response caused by increased NF-κB and the proinflammatory cytokine TNF-α, may be alleviated by C. botrys. Consequently, C. botrys could represent a potential therapeutic approach for patients with rhabdomyolysis-induced acute kidney injury.

Keywords: Chenopodium botrys; acute kidney injury; inflammation; rhabdomyolysis.

GRAPH 1

H NMR spectrum of the extract. The bottom line depicts the values of the integral areas.

FIGURE 1

Comparison of the serum albumin (A), creatinine (B), and urea (C) in experimental groups. Data are presented as mean ± SEM (n = 5 in each group). ^## p < 0.01 compared with the control group. *p < 0.05 compared with the glycerol group.

FIGURE 2

Comparison of the urine protein (A), creatinine (B), and urea (C) in experimental groups. Data are presented as mean ± SEM (n = 5 in each group).

FIGURE 3

Comparison of the total antioxidant capacity (A), NF‐κB ratio (B), and TNF‐α level (C) in experimental groups. Data are presented as mean ± SEM (n = 5 in each group). ^# p < 0.05 compared with the control group. *p < 0.05 and ***p < 0.001 compared with the glycerol group.

FIGURE 4

Sections of renal tissues stained with hematoxylin–eosin. (A) Glycerol group (cortex and medulla), (B) control group, (C) extract receiving group, and (D and E) treatment groups with extract and dexamethasone, respectively. The white arrow indicates glomerular/tubule granular degeneration, the brown arrows indicate tubule dilation, the gray arrow indicates cell vacuolization, the green arrow indicates hemorrhage/congestion, the red arrows indicate tubule pyknotic nucleus, the yellow arrow indicates tubule karyolitic nucleus, the blue arrow indicate tubule karyorrhexis nucleus, and the purple arrow indicates myoglobin cast. × 40 magnification.