Research Article Protective Effect of Joa-Gui Em through the Improvement of the NLRP3 and TLR4/NF-κb Signaling by Ischemia/Reperfusion-Induced Acute Renal Failure Rats Se Won Na, 1,2 Youn Jae Jang, 1,2 Mi Hyeon Hong, 1,2 Jung Joo Yoon, 1,2 Ho Sub Lee, 1,2 Hye Yoom Kim , 1,2 and Dae Gill Kang 1,2 1 College of Oriental Medicine and Professional Graduate School of Oriental Medicine, Wonkwang University, Iksan 54538, Republic of Korea 2 Hanbang Cardio-Renal Research Center and Professional Graduate School of Oriental Medicine, Wonkwang University, Iksan 54538, Republic of Korea Correspondence should be addressed to Hye Yoom Kim; hyeyoomc@naver.com and Dae Gill Kang; dgkang@wku.ac.kr Received 27 April 2021; Revised 14 May 2021; Accepted 20 May 2021; Published 28 May 2021 Academic Editor: Baotong Zhang Copyright © 2021 Se Won Na et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Joa-gui em ( , JGE) is known to be effective for treating kidney-yin deficient syndrome. However, there is a lack of objective pharmacological research on improving kidney function. is study was designed to evaluate whether JGE improves renal function and related mechanisms in rats with acute renal injury induced by ischemia/reperfusion (I/R). e acute renal failure (ARF) group was subjected to reperfusion after inserting a clip into the renal artery for 45 min. e ARF + JGE (100 or 200 mg/kg/ day) groups were orally administered for four days after their I/R surgery, respectively. JGE treatment suppressed the increase in kidney size in the ARF animal model and alleviated the polyuria symptoms. In addition, to confirm the effect of improving the kidney function of JGE, lactate dehydrogenase levels, blood urea nitrogen/creatinine ratio, and creatinine clearance were measured.Asaresult,itdecreasedintheARFgroupbutsignificantlyimprovedintheJGEgroup.Also,asaresultofexaminingthe morphological aspects of renal tissue, it was shown that JGE improved renal fibrosis caused by ARF. Meanwhile, it was confirmed that JGE reduced inflammation through the nucleotide-binding oligomerization domain-like receptor pyrin domain containing-3 (NLRP3) and toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathways, which are the major causes of acute ischemic kidney injury, thereby improving renal function disorder. e JGE has a protective effect by improving the NLRP3 and TLR4/NF-κB signaling pathway in rats with acute renal dysfunction induced by I/R injury. 1. Introduction e kidney is essential in maintaining homeostasis by regulating fluid volume through the excretion and reab- sorption of water. Ischemic kidney injury due to ischemia/ reperfusion (I/R) causes various kidney dysfunction, even- tually leading to acute renal failure (ARF). Moreover, kidney function is impaired, urine cannot be excreted normally, and the body loses its balance of water and electrolytes. e rapid increase in the levels of serum creatinine (Cr) decreases glomerular filtration in the kidneys [1]. It is widely assumed that ARF generally occurs due to acute tubular necrosis, usually due to ischemic renal injury [2]. ARF animal model has structural remodeling in the renal tubular epithelium [3, 4]. I/R-induced renal impairment significantly affects kidney function because the supply of reperfusion to the kidney causes a significant cellular metabolic disturbance and tissue inflammation [5, 6]. In inflammatory kidney diseases, the nucleotide-binding oligomerization domain- like receptor pyrin domain containing-3 (NLRP3) inflam- masome is a multi-protein complex induced by harmful factors in the body and plays an essential role in the in- flammatory response [7, 8]. Activation of NLRP3 inflam- masomes mediates the activation of caspase-1 and the secretion of inflammatory cytokines, including interleukin- (IL-) 1β and IL-18, resulting in a type of cell death called Hindawi Evidence-Based Complementary and Alternative Medicine Volume 2021, Article ID 7178868, 10 pages https://doi.org/10.1155/2021/7178868