INTERNATIONAL IMMUNOPHARMACOLOGY
·
2025
·
IF 4.7
Wenyang Zhou,Zhenhao Liu,Xichuan Qiu,Minghao Tian,Baoqiang He,Chao Tang,Qiang Tang,Rupei Ye,Dejun Zhong,Yehui Liao
Following spinal cord injury (SCI), pyroptosis plays a significant role in regulating neuroinflammation during the secondary phase of injury. Although 1,8-cineole possesses anti-inflammatory effects, its role in SCI and underlying molecular mechanisms remains unclear. This study revealed that 1,8-cineole promoted motor function recovery in spinal cord-injured rats, reduced NLRP3 inflammasome-mediated microglial pyroptosis and activation, enhanced neuronal regeneration, and suppressed neuronal apoptosis and glial scar formation. Network pharmacology analysis showed that 1,8-cineole targets the PI3K/AKT and P38 MAPK pathways to inhibit microglial activation and pyroptosis. Finally, using a conditional co-culture system, we demonstrated that 1,8-cineole-treated microglia facilitated neuronal regeneration while inhibiting apoptosis. These findings indicate that 1,8-cineole promotes functional recovery post-SCI by protecting neurons by suppressing microglial pyroptosis and activation through the PI3K/AKT and P38 MAPK axes.
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JOURNAL OF ETHNOPHARMACOLOGY
·
2024
·
IF 4.8
Qing-zhu Zhang,Hui-yuan Xu,Chao-yan Feng,Chu-hao Zhang,Kun Ren,Ying-ni Pan,Dong-mei Wang,Shu-meng Ren,Xiao-qiu Liu
Ethnopharmacological relevance The leaves of Quercus dentata Thunb. (QD), a member of the Fagaceae family and genus Quercus , with distributions in China, Japan, Korea, and other regions. As recorded in the Ben Cao Gang Mu (Compendium of Materia Medica) and other classical Chinese medical texts, QD has been traditionally employed in Traditional Chinese Medicine (TCM) for their hemostatic and diuretic effects and has been used to treat urinary stones ( Lin Zheng ). It is also the main ingredient of the Mishitong capsule (MST), a Chinese patent drug, used for kidney stones and ureteral stones. Nonetheless, the specific active ingredients and the mechanisms of QD in treating kidney stones remain to be elucidated, which is crucial for advancing the scientific understanding and clinical application of this traditional medicine. Aim of study This study aimed to identify the active constituents of QD water extract (QDWE), explore its inhibitory effects on kidney stones through in vitro and in vivo studies, and elucidate the underlying mechanisms of the OPN/CD44 axis and the NLRP3 signaling pathway to provide a full understanding of its potential as a novel treatment approach against kidney stones. Materials and methods The micromolecular components in the supernatant of QDWE (QDS) were analyzed by UPLC-Q-Exactive-Orbitrap-MS and the monosaccharide composition of the macromolecular polysaccharide components in the crude polysaccharide (QDP) was determined by pre-column derivatization in HPLC. The effects of QDWE, QDS and QDP on the shape, size, and structure of calcium oxalate (CaOx) crystals in vitro were explored by XRD, FTIR and SEM. The effects of QDWE, QDS and QDP on CaOx kidney stones in SD rats induced by ethylene glycol and VD 3 were compared in vivo . Furthermore, the underlying mechanisms of OPN/CD44 and NLRP3 pathways were investigated by Western blot analysis. Results There were 32 compounds identified in QDS. The monosaccharide composition ratio of QDP was Man: L-Rha: D-GlcA: D-GalA: D-Glc: D-Gal: L - Ara = 1.01: 22.52: 8.27: 38.61: 3.43: 17.80: 6.38, indicating a mixture of pectin-type acidic heteropolysaccharides. QDP had a more significant inhibitory effect on CaOx crystals in vitro than QDWE, which can inhibit the formation of CaOx monohydrate crystals (COM) and convert them into thermodynamically unstable CaOx dihydrate (COD) crystals. The high dose of QDWE exhibited significant in vivo efficacy ( P < 0.05), including anti-calculus, diuretic effects, and kidney protection, marked by decreased calcification and stone formation, alongside improved kidney vitality. Furthermore, the protective effects of QDWE were demonstrated to be associated with the OPN/CD44 and NLRP3 pathways. Conclusion The studies identified and analyzed the active constituents of QDWE. Among these, QDP significantly inhibited CaOx crystal generation in vitro and could be a potential component for the treatment of urinary stones in QDWE. Moreover, the results indicated that QDWE had a remarkable therapeutic effect on CaOx stones by modulating the OPN/CD44 axis to affect stone formation and the NLRP3 signaling pathway to mediate inflammation, providing an experimental basis for the mechanism of anti-urinary stone and deep development of QD.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2026
·
IF 8.5
Yu Cheng,Yao Wen,Zhaohan Wang,Lizhen Yang,Junming Liao,Jieyu Xing,Zheng Liu,Xiaoyan Sheng,Lingli Zhou,Sigui Zhou,Jian Zou,Haiyun Chen
Our previous investigations have revealed that Perilla frutescens -derived polysaccharide PFP50-1 exhibited significant neuroprotective activity by attenuating lipopolysaccharide (LPS)-induced neuroinflammatory responses in microglia. Nonetheless, the protection and mechanisms of its anti-neuroinflammatory activities are still poorly understood. The neuroprotection effects of PFP50-1's underlying mechanisms were evaluated in MPTP-stimulated Parkinson's disease (PD) mice and LPS-induced microglia, respectively. In vitro , PFP50-1 effectively suppressed the excessive release of pro-inflammatory cytokines. Meanwhile, PFP50-1 significantly downregulated the levels of Toll-like receptor 4 (TLR4), myeloid differentiation primary response protein gene 88 (MyD88), nuclear factor kappa-B (NF-κB), p-PI3K (phosphorylated phosphatidylinositol 3-Kinase), and p-Akt (phosphorylated Protein Kinase B). Subsequently, investigations revealed that TLR4 inhibitor (TAK242) and PI3K inhibitor (LY294002) significantly potentiated PFP50-1's inhibitory effects on LPS-induced pro-inflammatory mediators. Moreover, the excessive releases of Caspase-1, IL-18, and IL-1β were reversed by suppressing NLRP3 inflammasome activation. In conditioned medium-stimulated N2a cells, PFP50-1 exhibited a strong neuroprotective effect against neuroinflammation-mediated neurotoxicity by preventing MMP depolarization and ROS production. Notably, PFP50-1 effectively ameliorated MPTP-induced dopaminergic (DA) neuronal degeneration in vivo , which was associated with the downregulation of the TLR4-mediated and PI3K-mediated signaling pathways, as well as the NLRP3 inflammasome. Collectively, our data indicated that PFP50-1's anti-neuroinflammation effect is related to downregulating the TLR4/NF-κB and PI3K/Akt signaling pathways and suppressing NLRP3 inflammasome activation, making it a promising candidate for PD.
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Environment & Health
·
2026
·
IF 6.3
Shiyin Zhong,Qiongli Zhou,Jirui Yang,Zhimin Zhang,Xueting Chai,Jinghao Luo,Xin Zhang,Jingjing Liu,Yangzong Yixi,Lei Shi,Xuhong Chang,Hui Wang
Manganese (Mn) is an essential trace element, but increasing industrial and agricultural use has led to elevated levels of environmental Mn levels. Chronic overexposure to Mn can cause a Parkinson’s-like neurodegenerative disorder; however, the underlying mechanisms remain incompletely understood. This study combined in vitro and in vivo models to investigate the role of the cGAS–STING/NLRP3 axis in regulating the p38 MAPK/NF–κB pathway in the process of Mn-induced Tau aggregation leading to neurotoxicity. Our results demonstrated that MnCl2 exposure significantly activated both the cGAS–STING/NLRP3 signaling axis and the p38 MAPK/NF–κB pathway, accompanied by increased Tau expression. Genetic ablation of cGAS, STING, or NLRP3 attenuated Mn-induced Tau upregulation, indicating that the cGAS–STING/NLRP3 signaling axis mediates Tau expression. RNA-seq analysis further revealed that the decreased Tau expression in knockout cells is associated with the MAPK/NF–κB signaling pathway. Pharmacological inhibition of p38 MAPK or NF–κB markedly downregulated cGAS–STING signaling, inflammatory cytokine release, and phosphorylated Tau (p-Tau) levels. Moreover, we observed colocalization and interaction among p-p38, p-p65, and p-Tau. Overall, these findings reveal that Mn activates the cGAS–STING/NLRP3 signaling axis regulated by the p38 MAPK/NF–κB pathway, driving pathological Tau aggregation.
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Nutrients
·
2026
·Vol. 18
·期 14
·2360
·
IF 5.8
Xiaoxi Zhang,Gaoyang Fu,Xinyu Zhao,Yan Huang,Fenfen Li,Daozong Xia
Background/Objectives:Gouty arthritis (GA) is an inflammatory disease caused by increased purine metabolism. The limitations of current anti-GA therapies remain a major challenge. Astilbin, the main flavonoid in Smilax glabra Roxb., was found to exert potential anti-GA effects in our previous study.Methods:In this study, a mouse model of monosodium urate (MSU)-induced arthritis and an inflammatory model using mouse bone marrow-derived macrophages (BMDMs) were established.Results:Our data showed that astilbin reduced MSU-induced joint swelling and inflammatory infiltration in mice, restored lipopolysaccharide (LPS)/MSU-induced reductions in cell viability, and inhibited the expression levels of inflammatory factors IL-1β, IL-6 and TNF-α. Further studies showed that astilbin significantly reduced MSU-induced increases in NLRP3 and P-p65 protein levels, as well as the expression of ASC, P-IKKα, P-IκBα, and cleaved-caspase-1.Conclusions:This study suggests that astilbin may be a promising natural product for the treatment of GA by inhibiting the activation of the NLRP3 inflammasome and NF-κB signaling pathway.
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CYTOTECHNOLOGY
·
2026
·Vol. 78
·期 4
·156
·
IF 2.2
Zhang Yougen,Gu Li,Zhang Xiaoyang,Ran Wei,Yan Yanfeng,Gu Hongwei
Pulmonary inflammation is a key feature of chronic obstructive pulmonary disease (COPD), contributing to disease progression and morbidity. However, the molecular mechanisms underlying therapeutic interventions remain to be fully elucidated. This study aimed to investigate the mechanisms of naringenin in modulating COPD-related pulmonary inflammation. Using an integrated approach combining network pharmacology, molecular docking, and in vitro/in vivo models, we systematically explored the effects of naringenin. Network pharmacology analysis identified NF-κB as a central target, which was validated through molecular docking and dynamics simulations showing stable binding between naringenin and NF-κB. In vitro, cigarette smoke extract-challenged lung epithelial cells treated with naringenin exhibited reduced cytotoxicity, downregulated TNF-α, phospho-NF-κB p65, and NLRP3 expression, inhibited Caspase-1 activation, and attenuated IL-1β maturation, and suppressed Gasdermin D cleavage. In vivo, naringenin-treated COPD mice displayed diminished pulmonary inflammatory cell infiltration, milder histopathological lung damage, decreased serum TNF-α/IL-1β levels, and inhibited activation of the NF-κB/NLRP3/Caspase-1 axis in lung tissue. Collectively, these findings reveal that naringenin alleviates COPD pulmonary inflammation and pyroptosis by targeting the NF-κB/NLRP3/Caspase-1 signaling cascade, providing mechanistic insights for traditional Chinese medicine-based COPD therapies. Graphical abstract
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PROTEIN AND PEPTIDE LETTERS
·
2026
·Vol. 33
·期 1
·337-348
·
IF 1.1
Minghui Tian,Yemeng Zhang,Xiaolei Liu,Xiaoyu Liu,Wei Li
Introduction Polystyrene microplastics (PS-MPs) contribute to cardiovascular pathologies by inducing vascular endothelial injury through oxidative stress and inflammation. This study aimed to investigate the protective role of apricot kernel peptide extract (AKPE) against PS-MPs-induced damage in human aortic endothelial cells (HAECs) and to elucidate the underlying molecular mechanisms. Methods AKPE was isolated from apricot kernels using an activity-guided fractionation approach based on its protective efficacy in HAECs exposed to PS-MPs. Cytotoxicity and dose-response experiments established an optimal concentration of 20 μM. Subsequent analyses included cell viability (CCK-8 assay), intracellular reactive oxygen species (ROS) and superoxide dismutase (SOD) activity, inflammatory cytokine levels (α, IL-1β, IL-18) via ELISA, apoptosis assessment by flow cytometry, and evaluation of mitochondrial function. Bioactive oligopeptides within AKPE were identified by mass spectrometry. The involvement of the NLRP3 inflammasome and Wnt/β-catenin signaling pathways was examined using Western blotting and quantitative PCR. Results AKPE significantly counteracted the PS-MPs-induced reduction in HAEC viability, increasing it by 16.2% (p < 0.01). It also reduced intracellular ROS levels by 35.1% (p < 0.01) while preserving SOD activity. Furthermore, AKPE suppressed the production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-18) by 17–38% (p < 0.01). PS-MPs-induced mitochondrial dysfunction and apoptosis were markedly attenuated, with a 39.1% decrease in apoptotic cells (p < 0.01). Mass spectrometry identified eight key oligopeptides as the primary bioactive constituents of AKPE. Mechanistically, these components acted synergistically to inhibit NLRP3 inflammasome activation and to modulate the dysregulated Wnt/β-catenin pathway. Discussion AKPE protects HAECs from PS-MPs-induced damage through dual mechanisms: (1) suppressing NLRP3 inflammasome-driven inflammation and (2) mitigating oxidative stress via Wnt/β-catenin pathway inhibition. The synergy among AKPE peptides enhances resilience against PS-MPs, highlighting their potential as natural antioxidants. This study is the first to link apricot kernel peptides to PS-MPs-induced endothelial protection, providing novel insights into combating microplastic-related cardiovascular risks. Conclusion AKPE exerts potent protective effects against oxidative and inflammatory injury in HAECs caused by PS-MPs. These effects are mediated by its constituent bioactive oligopeptides, which concurrently regulate the NLRP3 inflammasome and Wnt/β-catenin signaling pathways. Our findings highlight AKPE's potential as a promising natural therapeutic agent for alleviating vascular endothelial damage associated with microplastic exposure.
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APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY
·
2026
·
IF 3.5
Li Tong,Li Ning,Li Yi,Liu Jinwen,Hao Dajie
Oxidative stress and inflammasome-driven inflammation are key contributors to atherosclerotic disease progression. Here, we report a ROS-responsive hyaluronic acid-PEGDA hydrogel designed for the sustained delivery of palmitoleic acid. In the study, catechol-functionalized hyaluronic acid was cross-linked with polyethylene glycol diacrylate to create an extracellular matrix mimic that possessed tunable mechanical strength and redox-sensitive degradability. It showed controlled release of palmitoleic acid under normal physiological conditions and a faster rate of release under oxidative conditions. In vitro studies using vascular endothelial cells and macrophages demonstrated good cytocompatibility and a marked reduction in intracellular reactive oxygen species, lipid peroxidation, and pro-inflammatory cytokine secretion. At the molecular level, treatment with the palmitoleic acid-loaded hydrogel resulted in activation of AMP-activated protein kinase, inhibition of NF-κB nuclear translocation, and suppression of NLRP3 inflammasome activation, as evidenced by decreased caspase-1 cleavage and IL-1β maturation. These findings indicate that ROS-responsive hydrogel-mediated delivery of palmitoleic acid effectively modulates oxidative and inflammatory signalling pathways relevant to atherosclerosis. Graphical
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JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Guangyan Li,Tongshu Wang,Yixuan Xie,Lu He,Huan Liu,Hongying Chen,Hong Jiang,Taoguang Huo
Ethnopharmacological relevance Realgar is extensively utilized in both modern medicine and traditional Chinese medicine. Although it has therapeutic uses, realgar exhibits hepatotoxicity, and improper use can result in liver inflammation and injury. The disruption of bile acid (BA) homeostasis, identified as an initiating event in liver injury, has been observed in the livers of realgar-exposed mice. However, the relationship between realgar-induced BA homeostasis imbalance and liver inflammation remains to be elucidated. Aim of the study To investigate the relationship between hepatic BA homeostasis disorder and liver inflammation caused by realgar exposure in mice, as well as the role and potential mechanism of intestinal farnesoid X receptor (FXR) in realgar-induced liver inflammation. Methods A sub-chronic realgar exposure mouse model was established and subjected to interventions with an intestinal-restricted FXR agonist or inhibitor. Plasma hepatic enzyme activities and total bile acid (TBA) levels were quantified using spectrophotometry. Hepatic inflammatory cytokine levels were analyzed by ELISA or RT-qPCR. Histopathological evaluation of liver injury was performed using HE staining. F4/80 expression was assessed via immunohistochemistry (IHC). Western blot (WB) and IHC were employed to examine the expression of proteins involved in the FXR-FGF15 axis, and plasma FGF15 concentrations were determined by ELISA. The expression of proteins related to enterohepatic circulation and the NLRP3 inflammasome pathway were evaluated using WB. Ultra-performance liquid chromatography coupled with time-of-flight mass spectrometry (UPLC-TOF-MS) was utilized to analyze BA profiles in both ileal and hepatic tissues. Results Our findings demonstrate that realgar exposure induces changes in ileal BA composition and subsequent suppression of the FXR-FGF15 signaling axis in mice. This axis suppression promotes hepatic BA overproduction and disrupts BA homeostasis in the livers of realgar-exposed mice, particularly elevates the levels of taurochenodeoxycholic acid (TCDCA) and taurolithocholic acid (TLCA). In vitro studies revealed that both TCDCA and TLCA can directly activate the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome in AML-12 cells, triggering pro-inflammatory cascades. Pharmacological activation of intestinal FXR effectively ameliorated realgar-induced hepatic inflammatory damage via restoring BA homeostasis and suppressing NLRP3 inflammasome activation. Conclusion Realgar exposure causes liver inflammatory injury by inducing BA-mediated NLRP3 inflammasome activation through down-regulating ileal FXR. Pharmacological activation of intestinal FXR alleviates realgar-induced liver inflammatory injury by restoring BA homeostasis and inhibiting BA-mediated NLRP3 inflammasome activation. These findings suggest that intestinal FXR may serve as a potential target for the prevention and treatment of realgar-induced liver injury.
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BIOMEDICINE & PHARMACOTHERAPY
·
2022
·
IF 7.419
Yao Liu,Ruifang Sun,XiaoPing Lin,Lanlan Wu,Hengying Chen,Siwen Shen,Yan Li,Yuanhuan Wei,Guifang Deng
Gestational Diabetes Mellitus (GDM) has an effect on the health of pregnant women and fetuses. Procyanidins (PA) is a flavonoid with anti-diabetic activity, but its effects and mechanisms on GDM have not been defined. Herein, we studied further the functions and mechanisms of PA on insulin resistance (IR) in GDM mice, as well as on postpartum and offspring mice. GDM mice model was built by feeding a high-fat-high-sucrose diet, and PA intervention (27.8 mg/kg/d) was performed from 4 weeks before pregnancy to delivery. Intestinal flora deficient (IFD) mice model was established by broad spectrum antibiotics. PA decreased the gestational weight gain, and the levels of fasting blood glucose, insulin, homeostasis model of assessment for IR index, yet increased the levels of HOMA for insulin sensitivity index. Interestingly, in IFD mice the effect of PA on improving IR was significantly weakened. PA inhibited inflammation by decreasing the levels of IL-6, TNF-α, IL-17 and CRP, which also been blocked in the IFD mice. Moreover, PA improved glycometabolism and reduced the secretion of inflammatory factors and hepatic inflammation infiltration of mice at 4 weeks postpartum, but had no significant effect on offspring mice. Mechanistically, PA treatment suppressed the nuclear factor‐κB (NF‐κB) p65 nuclear translocation and nucleotide‐binding domain like receptor protein 3 (NLRP3) inflammasome activation. In vitro studies, 4-hydroxyphenylacetic acid and 3-(4-hydroxyphenyl) propionic acid, main intestinal flora metabolites of PA restrained NF‐κB/NLRP3 activation. In conclusions, PA improved IR via NF-κB/NLRP3 pathway in GDM and postpartum mice, which partly through its metabolites by gut microbiome.
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Experimental and Therapeutic Medicine
·
2021
·Vol. 22
·期 5
·1-10
·
IF 2.447
Yan Zhou,Shuai Chen,Wenxian Gu,Xiao Sun,Linxiao Wang,Liming Tang
Sinomenine is a pure alkaloid that can be isolated from the root of Sinomenium acutum and has been found to exert anti‑inflammatory and immunosuppressive effects. The present study investigated the effects of sinomenine hydrochloride (SIN) on inflammation and the gut microbiota composition in the colon of mouse models of dextran sulfate sodium (DSS)‑induced colitis. DSS‑induced mice colitis was established by treating the mice with drinking water containing 3% (w/v) DSS for 7 days. The disease activity index of each mouse was calculated on a daily basis. All mice were sacrificed on day 11, then the weight of their spleen and length of their colons were measured. The histological analysis was measured by hematoxylin‑eosin staining. Oral administration of SIN (100 mg/kg/day) attenuated the DSS‑induced increases in the disease activity indices and spleen indices, DSS‑induced shortening of the colon length and histological damage. In addition, reverse transcription‑quantitative PCR data showed that SIN treatment effectively regulated the expression of inflammatory mediators, specifically by suppressing the expression of proinflammatory gene (TNF‑α, IL‑6 and inducible nitric oxide synthase) whilst increasing those associated with inhibiting inflammation (IL‑10 and arginine 1). Gut microbiota analysis was conducted using 16S ribosomal DNA sequencing. The results revealed that SIN improved bacterial community homeostasis and diversity, which were damaged by DSS. Furthermore, western blotting showed that the activation of the NOD‑, LRR‑ and pyrin domain‑containing protein 3 (NLRP3) inflammasome was markedly suppressed by SIN treatment. In conclusion, these results indicated that SIN may ameliorate experimental colitis by modulating the gut microbiota composition and suppressing the activation of the NLRP3 inflammasome in mice. Overall, these findings suggested a broad protective effect of SIN in treating inflammatory gut diseases, including ulcerative colitis.
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MEDIATORS OF INFLAMMATION
·
2021
·
IF 4.711
Qiang Zheng,Hang Zhao,Dong Jia,Xu Han,Zhenning Liu,Min Zhao
Paraquat (PQ) can cause multiorgan failure including acute kidney injury (AKI). Our prior study showed that Toll-interacting protein (TOLLIP) protected against PQ-induced acute lung injury. However, the role of TOLLIP in PQ-induced AKI remains undefined. This study was aimed at understanding the role and mechanism of TOLLIP in AKI. Six-eight-week-old male Wistar rats were intraperitoneally injected with 25 mg/kg PQ to induce AKI for 24 h in vivo. HK-2 cells were treated with 300 μM PQ for 24 h to induce cellular injury in vitro or 300 μM PQ and 5 μM nuclear factor-κB (NF-κB) inhibitor BAY11-7082 for 24 h. Rats were infected with adenovirus carrying TOLLIP shRNA via tail vein injection and HK-2 cells with adenovirus carrying TOLLIP shRNA or TOLLIP 48 h before PQ exposure. Results showed that TOLLIP and Toll-like receptor 2/4 (TLR2/4) expressions were boosted in the kidney after PQ intoxication. The toxic effect of PQ on the kidney and HK-2 cells was exacerbated by TOLLIP knockdown, as evidenced by aggravated glomerulus and tubule injury, inflammatory infiltration, and cell apoptosis in the kidney and increased loss of cell viability and apoptotic cells in HK-2 cells. TOLLIP knockdown also enhanced PQ-induced NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation in vivo and in vitro and TLR2/4-NF-κB signaling in vitro, reflected by increased contents of proinflammatory cytokines and expressions of NLRP3 inflammasome-related proteins in the kidney and HK-2 cells and expressions of TLR2, TLR4, and nuclear NF-κB p65 in HK-2 cells. However, TOLLIP overexpression inhibited PQ-induced loss of cell viability, cell apoptosis, NLRP3 inflammasome activation, and TLR2/4-NF-κB signaling in vitro. Additionally, BAY11-7082 abolished TOLLIP knockdown-induced NLRP3 inflammasome activation in vitro, indicating that TOLLIP protected against NLRP3 inflammasome activation in PQ-induced AKI through inhibiting TLR2/4-NF-κB signaling. This study highlights the importance of TOLLIP in AKI after PQ intoxication.
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