Mucosal-associated invariant T cells restrict reactive oxidative damage and preserve meningeal barrier integrity and cognitive function.

Increasing evidence indicates close interaction between immune cells and the brain, revising the traditional view of the immune privilege of the brain. However, the specific mechanisms by which immune cells promote normal neural function are not entirely understood. Mucosal-associated invariant T cells (MAIT cells) are a unique type of innate-like T cell with molecular and functional properties that remain to be better characterized. In the present study, we report that MAIT cells are present in the meninges and express high levels of antioxidant molecules. MAIT cell deficiency in mice results in the accumulation of reactive oxidative species in the meninges, leading to reduced expression of junctional protein and meningeal barrier leakage. The presence of MAIT cells restricts neuroinflammation in the brain and preserves learning and memory. Together, our work reveals a new functional role for MAIT cells in the meninges and suggests that meningeal immune cells can help maintain normal neural function by preserving meningeal barrier homeostasis and integrity.

Glycyrrhizin attenuates renal inflammation in a mouse Con A-hepatitis model via the IL-25/M2 axis.

Glycyrrhizin (GL) has immunoregulatory effects on various inflammatory diseases including hepatitis and nephritis. However, the mechanisms underlying the anti-inflammatory effect of GL on renal inflammation are not fully understood. Hepatorenal syndrome (HRS) is a functional acute renal impairment that occurs in severe liver disease, and we found that kidney injury also occurs in Con A-induced experimental hepatitis in mice. We previously found that GL can alleviate Con A-induced hepatitis by regulating the expression of IL-25 in the liver. We wanted to investigate whether GL can alleviate Con A-induced nephritis by regulating IL-25. IL-25 regulates inflammation by modulating type 2 immune responses, but the mechanism by which IL-25 affects kidney disease remains unclear. In this study, we found that the administration of GL enhanced the expression of IL-25 in renal tissues; the latter promoted the generation of type 2 macrophages (M2), which inhibited inflammation in the kidney caused by Con A challenge. IL-25 promoted the secretion of the inhibitory cytokine IL-10 by macrophages but inhibited the expression of the inflammatory cytokine IL-1ß by macrophages. Moreover, IL-25 downregulated the Con A-mediated expression of Toll-like receptor (TLR) 4 on macrophages. By comparing the roles of TLR2 and TLR4, we found that TLR4 is required for the immunoregulatory effect of IL-25 on macrophages. Our data revealed that GL has anti-inflammatory effects on Con A-induced kidney injury and that the GL/IL-25/M2 axis participates in the anti-inflammatory process. This study suggested that GL is a potential therapeutic for protecting against acute kidney injury.

The role of innate lymphocytes in regulating brain and cognitive function.

Mounting evidence indicates complex interaction between the immune system and the nervous system, challenging the traditional view about the immune privilege of the brain. Innate lymphoid cells (ILCs) and innate-like T cells are unique families of immune cells that functionally mirror traditional T cells but may function via antigen- and T cell antigen receptor (TCR)-independent mechanisms. Recent work indicates that various ILCs and innate-like T cell subsets are present in the brain barrier tissue, where they play important roles in regulating brain barrier integrity, brain homeostasis and cognitive function. In this review, we discuss recent advances in understanding the intricate roles for innate and innate-like lymphocytes in regulating brain and cognitive function.

Depletion of NK Cells Improves Cognitive Function in the Alzheimer Disease Mouse Model.

Despite mounting evidence suggesting the involvement of the immune system in regulating brain function, the specific role of immune and inflammatory cells in neurodegenerative diseases remain poorly understood. In this study, we report that depletion of NK cells, a type of innate lymphocytes, alleviates neuroinflammation, stimulates neurogenesis, and improves cognitive function in a triple-transgenic Alzheimer disease (AD) mouse model. NK cells in the brains of triple-transgenic AD mouse model (3xTg-AD) mice exhibited an enhanced proinflammatory profile. Depletion of NK cells by anti-NK1.1 Abs drastically improved cognitive function of 3xTg-AD mice. NK cell depletion did not affect amyloid ß concentrations but enhanced neurogenesis and reduced neuroinflammation. Notably, in 3xTg-AD mice depleted of NK cells, microglia demonstrated a homeostatic-like morphology, decreased proliferative response and reduced expression of neurodestructive proinflammatory cytokines. Together, our results suggest a proinflammatory role for NK cells in 3xTg-AD mice and indicate that targeting NK cells might unlock novel strategies to combat AD.

Interaction Between Innate Lymphoid Cells and the Nervous System.

The interaction between the immune system and the nervous system remains an intriguing enigma. Recent studies indicate that innate lymphoid cells (ILCs), a unique family of innate effector cells, participate in intense cross talk with the nervous system. In the mucosal barrier sites, ILCs have been found to co-localize with neurons, nerves, glial cell projectors, and neuroendocrine cells. The cross talk between ILCs and peripheral nervous system orchestrates mucosal homeostasis and immunity. In addition, the barrier tissues of the central nervous system (CNS) also provide conductive microenvironment for ILC development and maintenance. Activities of CNS-associated ILCs impact the outcome of various CNS disorders. In this chapter, we review and discuss the intricate and bidirectional interaction between ILCs and nervous system.

Group 2 innate lymphoid cells are numerically and functionally deficient in the triple transgenic mouse model of Alzheimer's disease.

BACKGROUND: The immune pathways in Alzheimer's disease (AD) remain incompletely understood. Our recent study indicates that tissue-resident group 2 innate lymphoid cells (ILC2) accumulate in the brain barriers of aged mice and that their activation alleviates aging-associated cognitive decline. The regulation and function of ILC2 in AD, however, remain unknown. METHODS: In this study, we examined the numbers and functional capability of ILC2 from the triple transgenic AD mice (3xTg-AD) and control wild-type mice. We investigated the effects of treatment with IL-5, a cytokine produced by ILC2, on the cognitive function of 3xTg-AD mice. RESULTS: We demonstrate that brain-associated ILC2 are numerically and functionally defective in the triple transgenic AD mouse model (3xTg-AD). The numbers of brain-associated ILC2 were greatly reduced in 7-month-old 3xTg-AD mice of both sexes, compared to those in age- and sex-matched control wild-type mice. The remaining ILC2 in 3xTg-AD mice failed to efficiently produce the type 2 cytokine IL-5 but gained the capability to express a number of proinflammatory genes. Administration of IL-5, a cytokine produced by ILC2, transiently improved spatial recognition and learning in 3xTg-AD mice. CONCLUSION: Our results collectively indicate that numerical and functional deficiency of ILC2 might contribute to the cognitive impairment of 3xTg-AD mice.

The predictive value of neutrophil-lymphocyte ratio at presentation for delayed neurological sequelae in carbon monoxide poisoning.

OBJECTIVE: To explore the predictive value of neutrophil-lymphocyte ratio (NLR) at presentation for delayed neurological sequelae (DNS) in carbon monoxide (CO) poisoning. METHODS: This single-center retrospective observational study included a total of 253 consecutive patients who visited the emergency department (ED) due to acute CO intoxication between 7 October 2015 and 31 December 2019. The included patients had a history of coma and their blood routine was measured within one hour of ED admission. They were divided into two groups according to the presence of DNS, including those who developed DNS (DNS group) and those who did not (non-DNS group). RESULTS: A total of 171 patients were included in this research, and 49 (28.7%) developed DNS. The median NLR at ED admission was obviously higher in the DNS group (10.60 [9.69-15.34]) than in the non-DNS group (7.53 [5.86-8.56]) (p < 0.001). Multivariate analysis indicated that a high NLR (adjusted odds ratio (AOR): 1.78, 95% confidence interval (CI): 1.46-2.18) and the occurrence of acute brain lesions (AOR: 7.50, 95%CI: 2.86-19.68) on diffusion-weighted imaging were independent predictors of DNS. The NLR was more than 8.97. The prediction of occurrence of DNS had a sensitivity of 93.88% and a specificity of 84.43%. Kappa value was 0.713. The predicted results showed good authenticity and consistency. CONCLUSION: The level of NLR at presentation had good predictive value for the development of DNS, showing the superior value for clinical application.

[Relationship between sleep disorders and hypertension in oil workers in Karamay City].

OBJECTIVE: To investigate the effect of sleep disorders on hypertension in oil workers and its mediating effect analysis. METHODS: Between June and September 2019, 1420 workers aged 20-60 years(745 males and 675 females; 384 aged 30 years, 563 aged 30-45 years and 473 aged 45 years) from six oilfield bases in Karamay City, Xinjiang Uygur Autonomous Region were surveyed using a two-stage randomized whole-group sampling method. Their current conditions, and the information on gender, age, ethnicity, personal monthly income, education level, job title, smoking, alcohol consumption, height, weight, and shift work of the oil workers were investigated by the basic questionnaire. The Pittsburgh Sleep Index was used to assess the sleep status, and the Logistic regression model was used to analyze the influencing factors of hypertension, and the Process program(version 3.3) was used to conduct the mediating effect model test. RESULTS: (1) The detection rate of sleep disorders was 52.5% and the prevalence of hypertension was 16.3%, with 21.6%(161) higher in women than 10.5%(71) in men(χ~2=31.877, P& lt; 0.001). The prevalence of hypertension increased with increasing age and body mass index(BMI)(χ~2=25.117, P& lt; 0.001), 20.1%(149) in the sleep disorder group were higher than 12.2%(83) in the non-sleep disorder group(χ~2=16.113, P& lt; 0.001). (2) After adjusting for gender, age, ethnicity, education, personal monthly income, smoking, alcohol consumption, shift work and BMI, sleep disorders(OR=1.686, 95% CI 1.232-2.308), gender(OR=1.565, 95% CI 1.035-2.367), age(OR_(30-45)=1.710, 95% CI 1.085-2.697; OR_(& gt; 45)=1.717, 95% CI 1.055-2.797), shift work(OR=2.698, 95% CI 1.889-3.855), BMI(OR_(24.0-27.9)=2.557, 95% CI 1.736-3.765; OR_(≥28.0)=4.001, 95% CI 2.553-6.318) increased the risk of hypertension. (3) The result of stratified analysis showed that with age(OR_(30-45)=1.642, 95% CI 1.019-2.645; OR_(& gt; 45)=1.998, 95% CI 1.223-3.263) and BMI(OR_(24.0-27.9)=1.652, 95% CI 1.079-2.528; OR_(≥28.0)=2.259, 95% CI 1.165-4.381) increased, the risk of hypertension due to sleep disorders increased. Sleep disorders(OR=2.002, 95% CI 1.336-2.936) were also risk factors for hypertension in the shift work group. (4) The result of the mediating effect test showed that there was a mediating effect(P& lt; 0.05) between sleep disorders in age(ß=0.240, Z=2.239), shift work(ß=0.656, Z=3.999), and BMI(ß=0.516, Z=7.258) and hypertension. CONCLUSION: Sleep disorders may be a risk factor affecting hypertension in oil workers in Karamay City, and there were mediating effects between age, shift work, and BMI and hypertension.

GDC-0941 and CXCL8 (3-72) K11R/G31P combination therapy confers enhanced efficacy against breast cancer.

Aim: Herein is presented the combined effect of PI3K inhibitor (GDC-0941) and CXCR1/2 analogue (G31P) in breast cancer. Materials & methods: Breast cancer cell lines and xenograft model were employed to test the efficacy of the combination therapy. Results: GDC-0941+G31P treatment substantially inhibited multiplication of all the breast cancer cell lines used in this study (BT474, HCC1954 and 4T1). Even though single therapies caused a meaningful S-phase cell cycle arrest, the inhibition effect was more potent with the combined treatment. Similarly, enhanced apoptosis accompanied GDC-0941+G31P treatment. Furthermore, the migration ability of the breast cancer cell lines were significantly curtailed by the combination therapy compared with the single treatments. Conclusion: The findings suggest that combination treatment involving PI3K inhibitor and CXCR1/2 analogue (G31P) could be a potent therapeutic option for breast cancer treatment.

Toll-like receptor 2 deficiency promotes the generation of alloreactive Th17 cells after cardiac transplantation in mice.

The emergence of alloreactive Th17 cells that mediate allograft rejection has provided an impetus to understand the factors affecting the generation of Th17 cells in allograft transplantation. How toll-like receptor 2 (TLR2) signalling regulates the generation of Th17 cells upon alloantigen stimuli remains unclear. In this study, we used a mouse model of cardiac allograft transplantation to investigate whether TLR2 signalling influences the development of Th17 cells. Here, we demonstrate that the TLR2-deficient recipient mice show high Th17 cells, both in spleens and allografts, as well as higher infiltrating inflammatory leukocytes in cardiac allografts compared to wild-type control recipient mice. mRNA expression of IL-17, IL-6, TNF-α, CCR6 and CCL20 within the allografts is markedly increased in TLR2-deficient recipient mice compared to wild-type recipient mice. In addition, TLR2 deficiency leads to upregulation of Signal transducer and activator of transcription 3 (STAT3) phosphorylation in both spleens and allografts. In an in vitro experiment, a mixed lymphocyte reaction was assessed, which further confirmed that TLR2 deficiency leads to a significant increase in the generation of Th17 cells compared with wild-type controls. Furthermore, IL-6 secreted by the dendritic cells of TLR2-deficient mice contributes to driving the generation of these Th17 cells. These results suggest that TLR2 signalling is important in regulating the development of Th17 cells after cardiac allograft transplantation.

CD8+ T cell/IL-33/ILC2 axis exacerbates the liver injury in Con A-induced hepatitis in T cell-transferred Rag2-deficient mice.

BACKGROUND: Previous studies showed that CD4+ T cells play a critical role in Con A-induced hepatitis in wild-type mice. However, the role of CD8+ T cells in the setting of Con A-induced hepatitis is enigmatic. The aim of study is to investigate the function of CD8+ T cells in the context of Con-A-induced hepatitis. MATERIALS AND SUBJECTS: Two different mouse models of Con A-induced hepatitis, T cell-transferred Rag2-/- mice and wild-type C57BL/6 mice, were used in the present study. IL-33 gene knockout mice were used to confirm the role of alarmin in Con A-induced hepatitis. RESULTS: Opposing to the previous results obtained in wild-type mice, transferred CD4+ T cells alone into Rag2-knockout mice cannot cause hepatitis upon Con A challenge. In stark contrast, transferred CD8+ T cells play an important role in the pathogenesis of Con A-induced liver injury in T cell-transferred Rag2-deficient mice. Furthermore, we found that hepatocytes injured by perforin-based CD8+ T cell cytotoxicity release the alarmin IL-33. This cytokine promotes ST2+ ILC2 development and the secretion of cytokines IL-5 and IL-13 to mediate liver inflammation triggered by Con A challenge. In addition, these type 2 cytokines, including those originated from CD4+ T cells, result in eosinophils accumulation in liver to exacerbate the liver injury after Con A administration. CONCLUSION: Our data for the first time revealed that CD8+ T cells play an indispensable role in the pathogenesis of Con A-induced liver injury in T cell-transferred Rag2-deficient mice. Therefore, the CD8+ T cell/IL-33/ILC2 axis is a potential therapeutic target for acute immune-mediated liver injury.

[Effect of occupational stress on hypertension in desert oilfield workers].

OBJECTIVE: To explore influence of occupational stress on hypertension in Xinjiang Uygur Autonomous Region desert oilfield workers. METHODS: Cluster sampling was applied. A total of 1280 petroleum workers from 3 oil fields were used in Karamay City, Xinjiang. Occupational Stress Scale(OSI-R) was used to evaluate occupational stress and analyze the impact of occupational stress on hypertension. RESULTS: With the increase of occupational stress, the prevalence rate of hypertension is increasing(χ~2=21. 078, P<0. 001). Multivariate analysis showed that the risk of high blood pressure in the occupational task was 1. 562 times(95%CI 1. 072-2. 277)as high as that of the less occupational group, and the risk of high blood pressure in the group with strong individual tension reaction was 1. 701 times(95%CI 1. 158-2. 498)as much as that of the weak group(P<0. 05). Analysis of influencing factors of hypertension showed that the risk of high blood pressure in the shift was 1. 389 times(95%CI 1. 115-1. 730)as high as those without the shift, in the frequent drinkers was 1. 877 times(95%CI 1. 300-2. 710)that of the non drinkers, in the high salt patients was 1. 286 times(95%CI 1. 107-1. 691)that of the low salt, in the obese was 1. 564 times(95%CI 1. 249-2. 216)that of the normal people, and in the highly occupational stress was 1. 976 times(95%CI 1. 641-2. 336)as high as the low occupational stress. CONCLUSION: Heavy occupational tasks and strong individual strain can increase the risk of hypertension in desert oilfield workers. Shift, drinking history, salt consumption, BMI and occupational stress were the influencing factors of hypertension in desert oilfield workers.

APE1 Asp148Glu polymorphism and lung cancer susceptibility.

Apurinic/apyrimidinic endonuclease 1 (APE1) is a key enzyme in base excision repair (BER) pathway for the removal of many oxidized and alkylated bases. Single-nucleotide polymorphisms of the APE1gene have been demonstrated to be involved in carcinogenesis. However, the association between APE1 Asp148Glu polymorphism and lung cancer risk remains inconclusive. To derive a precise estimate for this association, we carried out an updated meta-analysis by pooling data thus far published. The pooled odds ratio (OR) with 95 % confidence interval (95 % CI) was calculated to assess the role of APE1 Asp148Glu polymorphism in lung carcinogenesis. The pooled ORs suggested that variant genotypes of APE1 Asp148Glu were modestly associated with an elevated risk of lung cancer (GluGlu vs. AspAsp, OR=1.22, 95 % CI 1.01-1.48, P=0.038; GluGlu vs. AspAsp + AspGlu, OR=1.19, 95 % CI 1.02-1.39, P=0.023). The relationship was also observed in studies conducted among Asians, but not Caucasians. Sensitivity analysis further confirmed the findings. The meta-analysis shows that the polymorphism of APE1 Asp148Glu exerts risk effect on lung cancer development.

Polymorphisms in the vitamin D receptor gene and the lung cancer risk.

The relationship between the vitamin D receptor (VDR) polymorphisms and the susceptibility to lung cancer remains unclear. The present meta-analysis was performed to estimate the polymorphisms of VDR and lung cancer risk. The pooled odds ratios (ORs) and corresponding 95 % confidence intervals (CIs) were calculated. Subgroup analysis by smoking status was carried out for further elucidation. The VDR BsmI polymorphism seemed to be negatively associated with the lung cancer risk (A vs. G, OR = 0.71, 95 % CI, 0.52-0.96; GA vs. GG, OR = 0.54, 95 % CI, 0.35-0.83; AA + GA vs. GG, OR = 0.55, 95 % CI, 0.36-0.84), particularly among the smokers (AA + GA vs. GG, OR = 0.39, 95 % CI, 0.21-0.72). The VDR ApaI variant genotypes did not alter the risk of lung cancer under all gene models in overall analysis. However, smokers carrying the variant G allele were more susceptible to lung cancer (G vs. T, OR = 1.60, 95 % CI, 1.14-2.25). The polymorphism of VDR TaqI was related to a decreased risk of lung cancer (C vs. T, OR = 0.62, 95 % CI, 0.26-1.46; CC vs. TT, OR = 0.44, 95 % CI, 0.21-0.91; TC vs. TT, OR = 0.58, 95 % CI, 0.38-0.90; CC + TC vs. TT, OR = 0.55, 95 % CI, 0.36-0.84). Besides, the CC + TC carriers in the smokers were at a significantly reduced risk of lung cancer (CC + TC vs. TT, OR = 0.48, 95 % CI, 0.16-1.44). The study supports that the polymorphisms of VDR BsmI and TaqI play protective roles in the lung carcinogenesis, particularly among the smokers. The association of VDR ApaI polymorphism with the lung cancer risk needs to be further elucidated.

Exploring the Transmembrane Behaviors of Dietary Flavonoids under Intestinal Digestive Products of Different Lipids: Insights into the Structure-Activity Relationship In Vitro.

This study aimed to investigate the transmembrane transport behavior and structure-activity relationships of various dietary flavonoids in the presence of dietary lipids derived from different sources in vitro. Results revealed that the digestion products of soybean oil (SOED) and lard (LOED) augmented the apparent permeability coefficients of most dietary flavonoids, and SOED exhibited higher transport compared with LOED. The structural properties of flavonoids and the potential interactions between fatty acids in these digestion products and flavonoids may influence the outcomes. 3D quantitative structure-activity relationship analyses revealed that incorporating small-volume groups at position 8 of the A-ring augmented the transmembrane transfer of flavonoids in the LOED system compared with the control group. By contrast, the integration of hydrophobic groups at position 5 of the A-ring and hydrogen bonding acceptor groups at position 6 of the A-ring enhanced the transmembrane transportation of flavonoids in the SOED system. Molecular dynamics simulations revealed that the SOED system may facilitate the interactions with flavonoids to form more stable and compact fatty acid-flavonoid complexes compared to the LOED system. These findings may provide valuable insights into flavonoid absorption to facilitate the development and utilization of functional foods or dietary supplements based on dietary flavonoids.

A Wax Interface-Enabled One-Pot Multiplexed Nucleic Acid Testing Platform for Rapid and Sensitive Detection of Viruses and Variants.

High-quality, low-cost, and rapid detection is essential for the society to reopen the economy during the critical period of transition from Coronavirus Disease 2019 (COVID-19) pandemic response to pandemic control. In addition to performing sustainable and target-driven tracking of SARS-CoV-2, conducting comprehensive surveillance of variants and multiple respiratory pathogens is also critical due to the frequency of reinfections, mutation immune escape, and the growing prevalence of the cocirculation of multiple viruses. By utilizing a 0.05 cents wax interface, a Stable Interface assisted Multiplex Pathogenesis Locating Estimation in Onepot (SIMPLEone) using nested RPA and CRISPR/Cas12a enzymatic reporting system is successfully developed. This smartphone-based SIMPLEone system achieves highly sensitive one-pot detection of SARS-CoV-2 and its variants, or multiple respiratory viruses, in 40 min. A total of 89 clinical samples, 14 environmental samples, and 20 cat swab samples are analyzed by SIMPLEone, demonstrating its excellent sensitivity (3-6 copies/reaction for non-extraction detection of swab and 100-150 copies/mL for RNA extraction-based assay), accuracy (>97.7%), and specificity (100%). Furthermore, a high percentage (44.2%) of co-infection cases are detected in SARS-CoV-2-infected patients using SIMPLEone's multiplex detection capability.

Rhus chinensis Mill. fruits alleviate liver injury induced by isoniazid and rifampicin through regulating oxidative stress, apoptosis, and bile acid transport.

ETHNOPHARMACOLOGICAL RELEVANCE: Rhus chinensis Mill. is a species of the genus Rhus belonging to the family Anacardiaceae. Its fruits used to treat/prevent liver related diseases (e.g., jaundice and hepatitis) in folk medicine. Otherwise, the effects and underlying mechanisms of the fruits on the prevention of isoniazid and rifampicin-caused liver injury have not been investigated. AIM OF THE STUDY: To study the preventive effects and mechanisms of the Rhus chinensis Mill. fruits on isoniazid and rifampicin-caused liver injury. MATERIALS AND METHODS: This experiment was based on rifampicin (75 mg/kg/day) and isoniazid (75 mg/kg/day)-induced liver damage model to explain the pharmacological effects of Rhus chinensis Mill. fruits. The prevention of the extract from Rhus chinensis Mill. fruits on isoniazid and rifampicin-caused liver injury were evaluated using biochemical parameters, histopathological analysis, and immunofluorescence technique. Apart from that, the potential molecular mechanisms were elucidated by analyzing the expression of such crucial proteins participated in oxidative stress, apoptosis, and bile acid transport. RESULTS: The extract from Rhus chinensis Mill. fruits significantly reduced the levels of ALT, AST, TBIL, ALP and MDA. Besides, the extract, especially 800 mg/kg b.w., was remarkably decreased the content of TNF-α,IL-6 and IL-1ß, restored the levels of GSH and SOD. The results of Western blot also presented that the extract could activate the Nrf2 protein pathway and inhibit the expression of CYP2E1 to reduce oxidative stress. Meanwhile, the extract significantly up-regulated the expressions of BSEP and Mrp2 to regulate the transport of bile acid, and alleviated the cellular apoptosis via adjusting the expression of Bax and Bcl-2 proteins. CONCLUSIONS: Rhus chinensis Mill. fruits can prevent the liver injury induced by isoniazid and rifampicin in mice through adjusting the expressions of multiple proteins in oxidative stress, apoptosis, and bile acid transport pathways. This paper may provide scientific basis for the fruits as a Chinese medicine to prevent/cure liver injury.

The preventive effect of Chinese sumac fruit against monosodium urate-induced gouty arthritis in rats by regulating several inflammatory pathways.

Chinese sumac (Rhus chinensis Mill.) fruit is a traditional Chinese medicinal material that can be consumed daily. This study aimed to investigate whether the ethanol extract of sumac fruits can ameliorate monosodium urate-induced gouty arthritis in rats from the perspective of inflammation. Results showed that the extract of Chinese sumac fruits can obviously prevent monosodium urate-induced gouty arthritis in rats. Further analyses revealed that this bioactivity may be mainly achieved by modulating several inflammatory pathways, including NLRP3, NF-κB, and MAPK pathways. In addition, the extract can also improve oxidative stress by reducing the levels of malondialdehyde and myeloperoxidase, increasing the contents of superoxide dismutase and glutathione. In conclusion, this study revealed that the Chinese sumac fruit can alleviate the pathological symptoms of gouty arthritis by inhibiting inflammatory responses and oxidative stress, which can provide a theoretical basis for the use of Chinese sumac fruits as a Chinese herbal medicine and health food for the prevention and treatment of gouty arthritis.