Li Li

Li Li


Research Focus & Metrics

Academic Career Length

7Years (2020-Present)

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

Representative Publications

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1 October 2020 in Fitoterapia
Verified
Journal Article
Open access
TYTianmin Yuan
Tianmin Yuan
ZYZhujun Yin
Zhujun Yin
ZYZhixiang Yan
Zhixiang Yan
QHQing Hao
Qing Hao
JZJin Zeng
Jin Zeng
JZJunning Zhao
Junning Zhao
Diabetes is a worldwide healthy concern, which affects approximately 9% of the population. Tetrahydrocurcumin (THC) is the main metabolite of curcumin, which exerts the anti-diabetic activity. However, the underlying mechanism has not been clarified. In the research, we investigated whether THC could improve diabetes by regulating the gut microbiota and the expression of pancreatic glucagon-like peptide-1 (GLP-1) in the db/db mice. After 8-week THC administration (ig., once a day, THCH group: 200 mg/kg, THCL group: 100 mg/kg), the fasting blood glucose (FBG) was measured every two weeks. Serum insulin levels, the expression of GLP-1 in the pancreas, the histopathology of pancreas and the composition of gut microbiota were evaluated at the end of the experiment. Compared to the diabetic group, THC treatment decreased significantly blood glucose, increased the secretion of insulin and the expression of GLP-1 in the pancreas. Histomorphological analysis revealed that THC could protect pancreatic islet cells against hyperglycemic insult. Furthermore, the data from the sequencing of the 16S rDNA genes in gut microbiome displayed that THC could restore the intestinal dysbiosis, including the lowered relative abundance of Proteobacteria, Actinobacteria and the ratio of Firmicutes to Bacteroidetes. The linear regression analysis showed a close correlation between the GLP-1 expression and the proportion of the intestinal microflora. Altogether, these results demonstrated that THC might have a direct regulatory effect on gut microflora, which indirectly decrease the FBG levels by modulating GLP-1 expression in the pancreas.

31 August 2023 in Frontiers in Pharmacology
Verified
Journal Article
Open access
XZXin Zhu
Xin Zhu
YQYun-Yun Quan
Yun-Yun Quan
ZYZhu-Jun Yin
Zhu-Jun Yin
MLMin Li
Min Li
TWTing Wang
Ting Wang
LLLi Li
Li Li
Curcumae Longae Rhizoma (turmeric), Curcumae Radix and Curcumae Rhizoma are derived from the Curcuma species, and have gradually become three of the most commonly used medicinal herbs in China due to their different origins, processing methods and medicinal part. These three herbs have certain similarities in morphology, chemical composition, and pharmacological effects. All three of these herbs contain curcuminoids and volatile oil compounds, which exhibit anti-inflammatory, anti-tumor, antioxidant, and neuroprotective properties, although modern clinical applications have their own requirements. At present, there is no systematic guidelines for the clinical application of these three of Curcuma species; consequently, there is a high risk of unwanted phenomena associated with the mixing and indiscriminate use of these herbs. In this review, we focus predominantly on morphology, chemical composition, and the pharmacological activity of these three Curcuma herbs and summarize the current status of research in this field. Our goal is to provide a better understanding of clinical value of these Curcuma species so that we can provide reference guidelines for their further development, utilization and rational clinical application.

1 April 2021
Verified
Journal Article
Closed access
ZYZhujun Yin
Zhujun Yin
RTRuirong Tan
Ruirong Tan
TYTianmin Yuan
Tianmin Yuan
SCShilong Chen
Shilong Chen
YQYunyun Quan
Yunyun Quan
LLLi Li
Li Li

7 October 2022 in Evidence-Based Complementary and Alternative Medicine
Verified
Journal Article
Open access
PDF file
JLJirui Lang
Jirui Lang
LLLi Li
Li Li
SCShilong Chen
Shilong Chen
YQYunyun Quan
Yunyun Quan
JYJing Yi
Jing Yi
ZYZhujun Yin
Zhujun Yin
Background. Gout is a common crystal-related arthritis caused by the deposition of monosodium urates (MSU). Tibetan medicine Wuwei Shexiang Pills (WSP) has been demonstrated to exhibit anti-inflammatory, antihyperuricemia, and antigout activities. However, the underlying mechanism is unknown. Objectives. To explore the mechanisms of Wuwei Shexiang Pills on gouty arthritis via network pharmacology, molecule docking, and pharmacological verification. Methods. The ingredients and targets of WSP were obtained by searching and screening in BATMAN-TCM and SwissADME. The targets involving the gout were acquired from public databases. The shared targets were put onto STRING to construct a PPI network. Furthermore, Metascape was applied for the GO and KEGG enrichment analysis to predict the biological processes and signaling pathways. And molecular docking was performed to validate the binding association between the key ingredients and the relative proteins of TNF signaling. Based on the serum pharmacology, the predicted antigout mechanism of WSP was validated in MSU-induced THP-1 macrophages. The levels of inflammatory cytokines and mRNA were measured by ELISA and qRT-PCR, respectively, and MAPK, NF-κB, and NLRP3 signaling-associated proteins were determined by western blot and immunofluorescence staining. Results. 48 bioactive ingredients and 165 common targets were found in WSP. The data showed that 5-Cis-Cyclopentadecen-1-One, 5-Cis-Cyclotetradecen-1-One, ()-isoshyobunone, etc. were potential active ingredients. TNF signaling, HIF-1 signaling, and Jak-STAT signaling were predicted to be the potential pathways against gout. The molecule docking analysis found that most ingredients had a high affinity for p65, NLRP3, IL-1β, TNF-α, and p38. The data from in vitro experiment showed that WSP suppressed the production and gene expression of inflammatory cytokines. Furthermore, WSP could inhibit the activation of MAPK, NF-κB, and NLRP3 signaling pathways. Conclusion. Our finding suggested that the antigout effect of WSP could be achieved by inhibiting MAPK, NF-κB, and NLRP3 signaling pathways. WSP might be a candidate drug for gouty treatment.