Wei Huang

Affiliated Hospital of Southwest Medical University

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Yong Xu

Affiliated Hospital of Southwest Medical University

Chenlin Gao

Affiliated Hospital of Southwest Medical University

Youhua Xu

Macau University of Science and Technology

Luping Zhou

Affiliated Hospital of Southwest Medical University

Tingting Zhou

Southwest Medical University

Yang Long

Sichuan University

Junling Gu

Second People’s Hospital of Yibin

Yanqiu He

Affiliated Hospital of Southwest Medical University

Man Guo

Harbin Medical University

Yumei Xie

Affiliated Hospital of Southwest Medical University

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Affiliated Hospital of Southwest Medical University

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Southwest Medical University

First Affiliated Hospital of Sichuan Medical University

Sichuan University

Chinese Academy of Sciences

Nanjing University

University of Chinese Academy of Sciences

Macau University of Science and Technology

Chongqing Medical University

Southwest University

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Sodium Crotonate Alleviates Diabetic Kidney Disease Partially Via the Histone Crotonylation Pathway

Inflammation (2024)

Yanqiu He Yumei Xie Tingting Zhou Dongze Li Xi Cheng

10.1007/s10753-024-02047-w

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Citations (2)

The Proteasome Inhibitor, MG132, Attenuates Diabetic Nephropathy by Inhibiting SnoN DegradationIn VivoandIn Vitro

BioMed Research International (2014)

Wei Huang Yang Chen Qinling Nan Chenlin Gao Feng Hong

Transforming growth factor-β (TGF-β) has been shown to be involved in diabetic nephropathy (DN). The SnoN protein can regulate TGF-β signaling through interaction with Smad proteins. Recent studies have shown that SnoN is mainly degraded by the ubiquitin-proteasome pathway. However, the role of SnoN in the regulation of TGF- β/Smad signaling in DN is still unclear. In this study, diabetic rats were randomly divided into a diabetic control group (DC group) and a proteasome inhibitor (MG132) diabetes therapy group (DT group). Kidney damage parameters and the expression of SnoN, Smurf2, and TGF-β were observed. Simultaneously, we cultured rat glomerular mesangial cells (GMCs) stimulated with high glucose, and SnoN and Arkadia expression were measured. Results demonstrated that 24-hour urine protein, ACR, BUN, and the expression of Smurf2 and TGF- β were significantly increased (P < 0.05), whereas SnoN was significantly decreased in the DC group (P < 0.05). However, these changes diminished after treatment with MG132. SnoN expression in GMCs decreased significantly (P < 0.05), but Arkadia expression gradually increased due to high glucose stimulation (P < 0.05), which could be almost completely reversed by MG132 (P < 0.05). The present results support the hypothesis that MG132 may alleviate kidney damage by inhibiting SnoN degradation and TGF-β activation, suggesting that the ubiquitin-proteasome pathway may become a new therapeutic target for DN.

MG132

10.1155/2014/684765

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Citations (29)

Sodium butyrate supplementation ameliorates diabetic inflammation in db/db mice

Journal of Endocrinology (2018)

Youhua Xu Chenlin Gao Hengli Guo Wenqian Zhang Wei Huang

Endotoxemia has been recognized to be closely accompanied with type 2 diabetes mellitus (T2DM) and is responsible for many diabetic complications. Recent study suggests the potential role of butyrate, a short-chain fatty acid (SCFA) from microbiota metabolite, on T2DM. Gut-leak is a key event in diabetic-endotoxemia. To investigate if butyrate could ameliorate diabetic-endotoxemia, both in vivo and in vitro experiments were carried out in the present study. The effect of butyrate supplementation on blood HbA1c and inflammatory cytokines were determined in db/db mice; gut barrier integrity and expression of tight junction proteins were investigated both in vivo and in vitro . Oral butyrate administration significantly decreased blood HbA1c, inflammatory cytokines and LPS in db/db mice; inflammatory cell infiltration was reduced, and gut integrity and intercellular adhesion molecules were increased as detected by HE staining, immunohistochemistry and Western blot. By gut microbiota assay, ratio of Firmicutes:Bacteroidetes for gut microbiota was reduced by butyrate. In Caco-2 cells, butyrate significantly promoted cell proliferation, decreased inflammatory cytokines’ secretion, enhanced cell anti-oxidative stress ability and preserved the epithelial monocellular integrity, which was damaged by LPS. The present findings demonstrated that butyrate supplementation could ameliorate diabetic-endotoxemia in db/db mice via restoring composition of gut microbiota and preserving gut epithelial barrier integrity.

Proinflammatory cytokine

Sodium butyrate

10.1530/joe-18-0137

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Citations (126)

The Effects of Rhein and Honokiol on Metabolic Profiles in a Mouse Model of Acute Pancreatitis

Medical Science Monitor (2020)

Wei Huang Hang Liu Li Yu Gang Mai

BACKGROUND Acute pancreatitis (AP) is generally a self-limiting inflammatory disease, but is associated with a high mortality rate when severe. The present study aimed to investigate the effects of rhein and honokiol on AP. MATERIAL AND METHODS Thirty mice were randomly divided into 5 groups (n=6 per group): blank control, AP model, AP+rhein, AP+honokiol, and AP+rhein+honokiol. The AP model was prepared by intraperitoneal injection of cerulein and lipopolysaccharide (LPS). We observed the pathological changes of the pancreas by hematoxylin and eosin (H&E) staining. A mouse amylase kit was utilized to detect the level of amylase content in serum. Gas chromatography mass spectrometer analysis was performed to detect the differences in metabolites among the blank control, AP model, and AP+rhein+honokiol groups. RESULTS The serum amylase level was significantly higher in the AP model, which suggested that the AP model was constructed successfully. The AP+rhein+honokiol group had significantly reduced interstitial edema, inflammatory cell infiltration, hemorrhage, and necrosis. In addition, the rhein and honokiol treatment influenced some of the metabolic pathways in AP, including riboflavin metabolism, glycerophospholipid metabolism, linoleic acid metabolism, and the pentose and glucuronate interconversions pathway. CONCLUSIONS This study showed that the combination of rhein and honokiol ameliorated pathological changes in the pancreas of mice with AP.

Honokiol

Intraperitoneal injection

10.12659/msm.925727

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Citations (8)

Improved Indoor Localization With NLOS Signal Propagations

ICASSP 2022 - 2022 IEEE International Conference on Acoustics, Speech and Signal Processing (ICASSP) (2023)

Wei Huang Yixin Zhao Xuechao Wu Le Yin

This paper considers the indoor localization problem with possible non-line-of-sight (NLOS) signal propagations. Although centimeter-level accuracy can be achieved using ultrawideband (UWB) signal sources, NLOS propagation due to reflection and refraction of signals as well as multipath effect may lead to significant errors in UWB-based localization systems. To mitigate this issue, a novel and simple NLOS error compensation method is proposed in this paper, which introduces a correction factor that takes into account the influence of NLOS conditions on the UWB distance measurements. The inertial measurement unit (IMU) information are then used to correct the UWB distance measurements before passing them through a Kalman filter for data fusion. The effectiveness of the proposed approach over the state-of-the-art one is illustrated by both simulation and experiment.

Non-line-of-sight propagation

SIGNAL (programming language)

Reflection

10.1109/icassp49357.2023.10094695

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High Glucose-Induced Kidney Injury via Activation of Necroptosis in Diabetic Kidney Disease

Oxidative Medicine and Cellular Longevity (2023)

Man Guo Qing Chen Yongli Huang Qi Wu Yan Zeng

Diabetic kidney disease (DKD) is a major microvascular complication of diabetes mellitus (DM) and is closely associated to programmed cell death. However, the complex mechanisms of necroptosis, an alternative cell death pathway, in DKD pathogenesis are yet to be elucidated. This study indicates that necroptosis is involved in DKD induced by high glucose (HG) both in vivo and in vitro. HG intervention led to the activation of RIPK1/RIPK3/MLKL signaling, resulting in renal tissue necroptosis and proinflammatory activation in streptozotocin/high-fat diet- (STZ/HFD-) induced diabetic mice and HG-induced normal rat kidney tubular cells (NRK-52E). We further found that in HG-induced NRK-52E cell, necroptosis might, at least partly, depend on the levels of reactive oxygen species (ROS). Meanwhile, ROS participated in necroptosis via a positive feedback loop involving the RIPK1/RIPK3 pathway. In addition, blocking RIPK1/RIPK3/MLKL signaling by necrostatin-1 (Nec-1), a key inhibitor of RIPK1 in the necroptosis pathway, or antioxidant N-acetylcysteine (NAC), an inhibitor of ROS generation, could effectively protect the kidney against HG-induced damage, decrease the release of proinflammatory cytokines, and rescue renal function in STZ/HFD-induced diabetic mice. Inhibition of RIPK1 effectively decreased the activation of RIPK1-kinase-/NF-κB-dependent inflammation. Collectively, we demonstrated that high glucose induced DKD via renal tubular epithelium necroptosis, and Nec-1 or NAC treatment downregulated the RIPK1/RIPK3/MLKL pathway and finally reduced necroptosis, oxidative stress, and inflammation. Thus, RIPK1 may be a therapeutic target for DKD.

RIPK1

Proinflammatory cytokine

10.1155/2023/2713864

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Citations (15)

Short-Chain Fatty Acids Inhibit Oxidative Stress and Inflammation in Mesangial Cells Induced by High Glucose and Lipopolysaccharide

Experimental and Clinical Endocrinology & Diabetes (2017)

Wei Huang Hengli Guo Xian Deng Tingting Zhu Jianfeng Xiong

Recently, an connection between Short-chain fatty acids (SCFAs) produced by intestinal microbiota and kidney has been revealed. The aim of this study was to explore whether SCFAs or their specific G protein-coupled receptors 43 (GPR43) agonist inhibit oxidative stress and inflammatory response in glomerular mesangial cells (GMCs) induced by high glucose and lipopolysaccharide (LPS). Our research showed that treatment with SCFAs, especially acetate and butyrate, or GPR43 agonist significantly inhibited GMCs proliferation induced by high glucose and LPS, and then reversed the production of reactive oxygen species (ROS) and malondialdehyde (MDA) but increased levels of antioxidant enzyme superoxide dismutase (SOD). Furthermore, SCFAs or GPR43 agonist obviously increased the protein expression of GPR43 induced by high glucose and LPS, but diminished the expression of adhesion molecule intercellular adhesion molecule-1 (ICAM-1), and then decreased the proinflammatory cytokine monocyte chemoattractant protein (MCP-1) and interleukin-1β (IL-1β) release from GMCs stimulated by the high glucose and LPS. These combined results support the hypothesis that SCFAs or GPR43 agonist can inhibit oxidative stress and inflammation of GMCs induced by high glucose and LPS, suggesting that SCFAs induced signaling pathway may act as new therapeutic targets of diabetic nephropathy (DN).

Malondialdehyde

Proinflammatory cytokine

10.1055/s-0042-121493

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Citations (149)

iRhom2 promotes atherosclerosis through macrophage inflammation and induction of oxidative stress

Biochemical and Biophysical Research Communications (2018)

Chaohui Cheng Wei Huang Wen Hongfeng Yueliang Zhang Xiao-Qin Peng

Proinflammatory cytokine

10.1016/j.bbrc.2018.07.133

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Citations (21)

Sodium butyrate alleviates high-glucose-induced renal glomerular endothelial cells damage via inhibiting pyroptosis

International Immunopharmacology (2019)

Junling Gu Wei Huang Wenqian Zhang Tingting Zhao Chenlin Gao

Pyroptosis

Propidium iodide

Sodium butyrate

Proinflammatory cytokine

10.1016/j.intimp.2019.105832

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Citations (75)

496-P: A New Method to Image Sweet Taste Receptors in the Pathogenesis of Diabetic Nephropathy: Detection of 18F Lactisole with PET/CT

Diabetes (2019)

Luping Zhou Wei Huang Nan Liu Xiumin Ma Man Guo

Previous studies showed that the expression of sweet taste receptors (STRs) was obviously downregulated in the pathogenesis of diabetic nephropathy (DN), suggesting that STRs may act as new therapeutic targets of DN. However, STRs are weakly expressed in kidneys, it is necessary to find a non-invasive method for detection of STRs distribution in the whole body and kidney. Lactisole, a broad-acting sweet antagonist, is commercially available and may be useful to assess the function and physiological role of the STRs. Whether the detection of isotope 18F labeled lactisole (18F-lactisole) with PET/CT can be used as a probe for imaging STRs expression differences is unclear. In this study, DN mouse model was induced by streptozotocin (STZ) in vivo, mouse glomerular mesangial cells (GMCs) and human proximal tubular cells (HK-2) were stimulated by high glucose in vitro, exogenous lactisole was used as an intervention reagent, 18F-lactisole was used as probe agent to evaluate the expression and distribution of STRs in the pathogenesis of DN. Our results showed that both the expression and distribution of STRs in mice were clearly imaged by PET/CT via intravenous injection of 18F-lactisole, 18F-lactisole signal in renal tissue was attenuated under the condition of diabetes, this trend persisted 2 hours after furosemide injection. Furthermore, exogenous lactisole significantly mitigated the effect of high glucose on STRs in vitro and vivo, which were detected by PET/CT or radioactive dosimeter via 18F-lactisole. These combined results support the hypothesis that detection of 18F-lactisole with PET/CT can be used as a new probe to image STRs and distinguish its expression level, suggesting a new method for non-invasive diagnosis of DN. Disclosure L. Zhou: None. W. Huang: None. N. Liu: None. X.M. Ma: None. M. Guo: None. Q. Chen: None. C. Gao: None. Y. Xu: None.

Pathogenesis

10.2337/db19-496-p

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Citations (1)