Shenghua Piao

Shenghua Piao


Research Focus & Metrics

Academic Career Length

5Years (2022-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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13 September 2022 in Frontiers in Endocrinology
Verified
Journal Article
Open access
LLLirong Lei
Lirong Lei
NZNing Zhao
Ning Zhao
LZLei Zhang
Lei Zhang
JCJiamei Chen
Jiamei Chen
XLXiaomin Liu
Xiaomin Liu
SPShenghua Piao
Shenghua Piao
Dyslipidemia, as a common metabolic disease, could cause atherosclerosis, coronary heart disease, stroke and other cardio-cerebrovascular diseases. It is mainly caused by the interaction of genetic and environmental factors and its incidence has increased for several years. A large number of studies have shown that gut microbiota disorder is related to the development of dyslipidemia closely. Especially its metabolites such as short-chain fatty acids, bile acids and trimethylamine N-oxide affect dyslipidemia by regulating cholesterol balance. In this paper, we systematically reviewed the literature and used knowledge graphs to analyze the research trends and characteristics of dyslipidemia mediated by gut microbiota, revealing that the interaction between diet and gut microbiota leads to dyslipidemia as one of the main factors. In addition, starting from the destruction of the dynamic balance between gut microbiota and host caused by dyslipidemia, we systematically summarize the molecular mechanism of gut microbiota regulating dyslipidemia and provide a theoretical basis for the treatment of dyslipidemia by targeting the gut microbiota.

15 January 2024 in Journal of Ethnopharmacology
Verified
Journal Article
Open access
XSXiaoqi Shao
Xiaoqi Shao
WZWenru Zeng
Wenru Zeng
QWQing Wang
Qing Wang
SLSuping Liu
Suping Liu
QGQiaoling Guo
Qiaoling Guo
JGJiao Guo
Jiao Guo
Research on the Chinese herbal formula Fufang Zhenzhu Tiaozhi (FTZ) has demonstrated its effectiveness in treating hyperlipidemia and glycolipid metabolic disorders. Additionally, FTZ has shown inhibitory effects on oxidative stress, regulation of lipid metabolism, and reduction of inflammation in these conditions. However, the precise mechanisms through which FTZ modulates macrophage function in atherosclerosis remain incompletely understood. Therefore, this study aims to investigate whether FTZ can effectively stabilize rupture-prone plaques by suppressing macrophage pyroptosis and impeding the development of M1 macrophage polarization in ApoE-/- mice. To assess the impact of FTZ on macrophage function and atherosclerosis in ApoE-/- mice, we orally administered FTZ at a dosage of 1.2 g/kg body weight daily for 14 weeks. Levels of interleukin-18 and interleukin-1β were quantified using ELISA kits to gauge FTZ's influence on inflammation. Total cholesterol content was measured with a Cholesterol Assay Kit to evaluate FTZ's effect on lipid metabolism. Aortic tissues were stained with Oil Red O, and immunohistochemistry techniques were applied to assess atherosclerotic lesions and plaque stability. To evaluate the effects of FTZ on macrophage pyroptosis and oxidative damage, immunofluorescence staining was utilized. Additionally, we conducted an analysis of protein and mRNA expression levels of NLRP3 inflammasome-related genes and macrophage polarization-related genes using RT-PCR and western blotting techniques. This study illustrates the potential therapeutic effectiveness of FTZ in mitigating the severity of atherosclerosis and improving serum lipid profiles by inhibiting inflammation. The observed enhancements in atherosclerosis severity and inflammation can be attributed to the suppression of NLRP3 inflammasome activity and M1 polarization by FTZ. The current findings indicate that FTZ provides protection against atherosclerosis, positioning it as a promising candidate for novel therapies targeting atherosclerosis and related cardiovascular diseases.

7 October 2024 in Diabetology & Metabolic Syndrome
Verified
Journal Article
Open access
PDF file
ZZZhipeng Zhou
Zhipeng Zhou
MXMingyue Xu
Mingyue Xu
PXPingjie Xiong
Pingjie Xiong
JYJing Yuan
Jing Yuan
DZDeqing Zheng
Deqing Zheng
SPShenghua Piao
Shenghua Piao
Latent Autoimmune Diabetes in Adults (LADA) is a type of diabetes mellitus often overlooked in clinical practice for its dual resemblance to Type 1 Diabetes Mellitus (T1DM) in pathogenesis and to Type 2 Diabetes Mellitus (T2DM) in clinical presentation. To better understand LADA’s distinctiveness from T1DM and T2DM, we conducted a comprehensive review encompassing etiology, pathology, clinical features, treatment modalities, and prognostic outcomes. With this comparative lens, we propose that LADA defies simple classification as either T1DM or T2DM. The specific treatments for the disease are limited and should be based on the therapies of T1DM or T2DM that address specific clinical issues at different stages of the disease. It is crucial to identify LADA cases potentially misdiagnosed as T2DM, warranting prompt screening for poor blood sugar control, short-term blood sugar deterioration, and other conditions. If the prognosis for LADA is similar to T2DM, it can be managed as T2DM. However, if the prognosis fundamentally differs, early LADA screening is crucial to optimize patient outcomes and enhance research on tailored treatments. The pathogenesis of LADA is clear, so the prognosis may be the key to determining whether it can be classified as T2DM, which is also the direction of future research. On the one hand, this paper aims to provide suggestions for the clinical screening and treatment of LADA based on the latest progress and provide worthy directions for future research on LADA.

17 September 2025 in Frontiers in Nutrition
Verified
Journal Article
Open access
PDF file
WWWanchun Wang
Wanchun Wang
EZEnzheng Zhu
Enzheng Zhu
YYYang Yang
Yang Yang
QHQingqing Huang
Qingqing Huang
XXXue Xiao
Xue Xiao
SPShenghua Piao
Shenghua Piao
Introduction: The high-fat and high-fructose diet (HFFD) can lead to various metabolic disorders. Pangxiejiao (PXJ), a natural plant widely used in folk practices, has been found to contain bioactive compounds that exhibit hypoglycemic effects in vitro. However, the potential of PXJ aqueous extract to ameliorate metabolic disorders in vivo and its underlying mechanisms remain unexplored. This study aims to investigate the effects of PXJ on metabolic disorders induced by HFFD in rats.Methods: An HFFD was employed to mimic unhealthy dietary habits, while PXJ was administered via oral gavage for 10 weeks. Perform biochemical assays, observe histopathological structures, and evaluate metabolic status in rats to investigate intrinsic alterations through detection of gut microbiota and plasma metabolites.Results: The results demonstrated that PXJ intervention reduced body weight, improved glucose and lipid metabolism, and decreased serum uric acid levels. PXJ alleviated oxidative stress and inflammation, as evidenced by reduced serum levels of IL-1β, IL-6, and TNF-α, along with ameliorated pathological inflammatory manifestations in metabolism-related organs, such as liver, pancreas, and colon. Furthermore, PXJ was found to decrease the Firmicutes/Bacteroidota ratio, modulated gut microbiota composition, and maintain microbial homeostasis. Nontargeted metabolomics analysis identified 39 upregulated metabolites, including hippuric acid, and 9 downregulated metabolites, such as LysoPG(18:2(9Z,12Z)/0:0). Correlation analysis further revealed that PXJ maintains metabolic homeostasis through complex network crosstalk. Specifically, four gut microbial taxa including Alloprevotella and six metabolites, including hippuric acid, demonstrated significant negative correlations with IL-6, TNF-α, and MDA. In contrast, Lachnospiraceae_NK4A136_group showed positive correlations with these metabolites and SOD.Discussion: In conclusion, early and sustained PXJ intervention alleviates HFFD-induced metabolic disorders, which is associated with restored gut microbiota balance, improved metabolism, and reduced inflammation and oxidative stress, demonstrating its potential as a novel functional tea for metabolic disorder prevention.