1.Antagonist of leukotriene B4 receptor 1 attenuates cisplatin induced acute kidney injury in mice and its associated mechanism
Bo DENG ; Yuli LIN ; Shuai MA ; Rui HE ; Feng DING
Chinese Journal of Nephrology 2015;31(5):345-350
Objective To investigate the effect of pretreatment with U75302,antagonist of leukotriene B4 receptor 1 (BLT1),on cisplatin induced acute kidney injury in mice and its immunoregulatory mechanism.Methods Healthy C57BL/6 mice were randomized into four subgroups:1.healthy control group;2.cisplatin group;3.U75302 control group;4.cisplatin + U75302 group,n=6.Group 2 and 4 received intraperitoneal injection of cisplatin (20 mg/kg) on day 0,group 3 and 4received intraperitoneal injection of U75302 (5 μg/mouse) on day 0 and day 2.Mice were sacrificed on the 3rd day and blood and kidney were collected.Renal function and histological changes were estimated,the infiltration of immune cells were determined by flow cytometry,the level of peroxidase (MPO) in kidney were determined by colorimetry,relative expression of TNF-α,IL-1β,CXCL1,CXCL2 were detected by Real-time PCR.Results Compared with healthy control group,levels of BUN,Scr were higher in cisplatin group with serious tubular structural damage.There were more neutrophils,macrophages,CD4+ T lymphocytes,CD8+ T lymphocytes in kidneys of cisplatin group,the level of MPO and relative expression of TNF-α,IL-1β,CXCL1,CXCL2 were also higher in cisplatin group.Compared with cisplatin group,lower BUN [(17.75±1.80) mmol/L vs (42.6±6.66) mmol/L,P <0.05],Scr were found in cisplatin+ U75302 group with less tubular structural damage.Meanwhile,U75302 reduced infiltration of neutrophils [(146±13)×103/g vs (296±66) ×103/g,P < 0.05],macrophages [(245± 13)× 103/g vs (420±78)× 103/g,P < 0.05] in the kidney.Levels of MPO [(1.756±0.283) U/g vs (3.308±0.577) U/g,P<0.05] and relative expression of TNF-α,IL-1β,CXCL1,CXCL2 were also lower.Conclusions BLT1 antagonist U75302 protects mice against AKI induced by cisplatin,and the mechanism is associated with reduced infiltration of inflammatory cells in kidney and the inhibition of kidney inflammation.
2.Clinical Observation on 48 Cases of Peripheral Facial Paralysis Treated by Acupoint-penetrating Acupuncture
Xin DENG ; Chunling BAO ; Yuli ZHANG ; Guirong DONG ; Guoqi HUANG
Journal of Acupuncture and Tuina Science 2006;4(3):189-190
In the treatment of 48 cases of peripheral facial paralysis by puncturing Yangbai (GB 14)toward Yuyao (Ex-HN 4), Dicang (ST 4) toward Jiache (ST 6), Xiaguan (ST 7) toward Jiache (ST 6),Sibai (ST 2) toward Quanliao (SI 18), Baihui (GV 20) toward Taiyang (Ex-HN 5), Yintang (Ex-HN 3)toward Shangen (Ex-HN), Cuanzhu (BL 2) toward Jingming (BL 1), and Hegu (LI 4) toward Laogong (PC 8) on the sick side, with other acupoints added in accordance with the symptoms, the results showed cure in 39 cases, remarkable effect in 7 cases, failure in 2 cases, and the curative rate in 81.2% and the effective rate in 95.8%.
3.Collagen/bioactive glass/chitosan composite scaffolds
Yongchun MENG ; Xiaofeng CHEN ; Kaihui NAN ; Yuli LI ; Xiaogang LUO ; Chunlin DENG
Chinese Journal of Tissue Engineering Research 2014;(21):3367-3373
BACKGROUND:Col agen/bioactive glass composite materials possess excellent osteogenic potential and biocompatibility, but its application in bone tissue engineering is limited by mechanical property and degradation. OBJECTIVE:To construct col agen/bioactive glass/chitosan composite scaffolds with good mechanical property, anti-degradation ability and bone repair property.
METHODS:Bioactive glass/col agen composite scaffolds with chitosan as dispersant were prepared by lyophylization. Fourier transform infrared spectroscopy, scanning electron microscope, X-ray diffraction, and dynamic biomechanical testing were used to characterize the structure and properties of the composite scaffolds. RESULTS AND CONCLUSION:Results show that charge-attractions in pre-prepared bioactive glass/chitosan solution increased the homogeneity of bioactive glass dispersed in col agen gel and the compressive modulus and strength increased significantly due to the homogeneity and intermolecular interactions between chitosan and col agen. The enzymatic degradation rate and mineralization activity in the simulated body fluid were also lower because of a high degree of embedment of bioactive glass in col agen/chitosan matrix, and entanglement of col agen in chitosan at molecular level, which decreased the exposure of bioactive glass to the simulated body fluid, and col agen to enzyme solution.
4.Clinical observation of TNF-α content in nasopharyngeal secretion of patients with nasopharyngeal carcinoma
Dewei CUI ; Yulan ZHAO ; Yuli DENG ; Guoqing LUO ; Min SU ; Xiangyang CHEN
Journal of Clinical Otorhinolaryngology Head and Neck Surgery 2001;(5):202-203
Objective:To detect the changes of tumor necrosis factor-α(TNF-α) in nasopharyngeal secretion of patients with nasopharyngeal carcinoma(NPC).Method: The content of TNF-α in nasopharyngeal secretion was determined by radioimmunoassay (RIA) in 20 controls,52 patients with NPC.Result:The average concentrations of TNF-α were (12.95±4.62)pmol/L in control group,(33.68±15.13) pmol/L in NPC group and (64.00±11.57)pmol/L in NPC with necrosis group. The content of TNF-α in nasopharyngeal secretion in control group was lower significantly than that of patients with NPC (P<0.01).Conclusion:The level of TNF-α in nasopharyngeal secretion of NPC patients was higher than that of normal subjects. To detect the content of TNF-α in nasopharyngeal secretion is a useful test for the study and diagnosis of NPC.
5.YTE-17 inhibits colonic carcinogenesis by resetting antitumor immune response via Wnt5a/JNK mediated metabolic signaling
Sui HUA ; Deng WANLI ; Chai QIONG ; Han BING ; Zhang YULI ; Wei ZHENZHEN ; Li ZAN ; Wang TING ; Feng JILING ; Yuan MAN ; Tang QINGFENG ; Xu HONGXI
Journal of Pharmaceutical Analysis 2024;14(4):525-541
The density and composition of lymphocytes infiltrating colon tumors serve as predictive factors for the clinical outcome of colon cancer.Our previous studies highlighted the potent anti-cancer properties of the principal compounds found in Garcinia yunnanensis(YTE-17),attributing these effects to the regu-lation of multiple signaling pathways.However,knowledge regarding the mechanism and effect of YTE-17 in the prevention of colorectal cancer is limited.In this study,we conducted isobaric tags for relative and absolute quantification(iTRAQ)analysis on intestinal epithelial cells(IECs)exposed YTE-17,both in vitro and in vivo,revealing a significant inhibition of the Wnt family member 5a(Wnt5a)/c-Jun N-terminal kinase(JNK)signaling pathway.Subsequently,we elucidated the influence and mechanism of YTE-17 on the tumor microenvironment(TME),specifically focusing on macrophage-mediated T helper 17(Th17)cell induction in a colitis-associated cancer(CAC)model with Wnt5a deletion.Additionally,we performed the single-cell RNA sequencing(scRNA-seq)on the colonic tissue from the Wnt5a-deleted CAC model to characterize the composition,lineage,and functional status of immune mesenchymal cells during different stages of colorectal cancer(CRC)progression.Remarkably,our findings demon-strate a significant reduction in M2 macrophage polarization and Th17 cell phenotype upon treatment with YTE-17,leading to the restoration of regulatory T(Treg)/Th17 cell balance in azoxymethane(AOM)/dextran sodium sulfate(DSS)model.Furthermore,we also confirmed that YTE-17 effectively inhibited the glycolysis of Th17 cells in both direct and indirect co-culture systems with M2 macrophages.Notably,our study shed light on potential mechanisms linking the non-canonical Wnt5a/JNK signaling pathway and well-established canonical β-catenin oncogenic pathway in vivo.Specifically,we proposed that Wnt5a/JNK signaling activity in IECs promotes the development of cancer stem cells with β-catenin activity within the TME,involving macrophages and T cells.In summary,our study undergoes the po-tential of YTE-17 as a preventive strategy against CRC development by addressing the imbalance with the immune microenvironment,thereby mitigating the risk of malignancies.