Abstract
Acute kidney injury (AKI) is a common complication of sepsis and has also been observed in some patients suffering from the new coronavirus pneumonia COVID-19, which is currently a major global concern. Thymoquinone (TQ) is one of the most active ingredients in Nigella sativa seeds. It has a variety of beneficial properties including anti-inflammatory and antioxidative activities. Here, we investigated the possible protective effects of TQ against kidney damage in septic BALB/c mice. Eight-week-old male BALB/c mice were divided into four groups: control, TQ, cecal ligation and puncture (CLP), and TQ+CLP. CLP was performed after 2 weeks of TQ gavage. After 48 h, we measured the histopathological alterations in the kidney tissue and the serum levels of creatinine (CRE) and blood urea nitrogen (BUN). We also evaluated pyroptosis (NLRP3, caspase-1), apoptosis (caspase-3, caspase-8), proinflammatory (TNF-α, IL-1β, and IL-6)-related protein and gene expression levels. Our results demonstrated that TQ inhibited CLP-induced increased serum CRE and BUN levels. It also significantly inhibited the high levels of NLRP3, caspase-1, caspase-3, caspase-8, TNF-α, IL-1β, and IL-6 induced by CLP. Furthermore, NF-κB protein level was significantly decreased in the TQ+CLP group than in the CLP group. Together, our results indicate that TQ may be a potential therapeutic agent for sepsis-induced AKI.
Highlights
There was a rapid increase in the number of COVID-19 cases worldwide; this pandemic caused by a new human coronavirus is of global concern [1, 2]
At 48 h after cecal ligation and puncture (CLP) injury, we observed a significant increase in serum blood urea nitrogen (BUN) and CRE levels in the CLP group than in the control group, but treatment of TQ significantly decreased serum BUN and CRE levels
The CLP group showed the infiltration of inflammatory cells into the kidney tissue, which could be ameliorated by treatment with TQ
Summary
There was a rapid increase in the number of COVID-19 cases worldwide; this pandemic caused by a new human coronavirus is of global concern [1, 2]. AKI is a serious complication of sepsis associated with high morbidity and mortality [4, 5]. Increasing evidence suggests that oxidative stress, hypoxia, intrarenal inflammatory response, and renal cell apoptosis are the main mechanisms of sepsis-related renal injury [6]. Antioxidant, anti-inflammatory, and immunomodulatory effects of TQ against renal damage have been demonstrated [8, 9]. Farooqui et al reported that oral administration of TQ effectively mitigated the renal damage caused by cisplatin-generated free radical attack [11]. Another study indicated that TQ could ameliorate renal toxicity induced by a high-dose diclofenac treatment [12]. The role of TQ in sepsis-induced AKI is not known. We established the model of sepsis-induced AKI in BALB/c mice and investigated the effect and mechanism(s) of TQ on sepsis-induced AKI
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