Publications by authors named "Shunjun Jiang"

7 Publications

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Mibefradil and Flunarizine, Two T-Type Calcium Channel Inhibitors, Protect Mice against Lipopolysaccharide-Induced Acute Lung Injury.

Mediators Inflamm 2020 10;2020:3691701. Epub 2020 Nov 10.

Department of Pharmacy, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China.

Recent studies have illuminated that blocking Ca influx into effector cells is an attractive therapeutic strategy for lung injury. We hypothesize that T-type calcium channel may be a potential therapeutic target for acute lung injury (ALI). In this study, the pharmacological activity of mibefradil (a classical T-type calcium channel inhibitor) was assessed in a mouse model of lipopolysaccharide- (LPS-) induced ALI. In LPS challenged mice, mibefradil (20 and 40 mg/kg) dramatically decreased the total cell number, as well as the productions of TNF- and IL-6 in bronchoalveolar lavage fluid (BALF). Mibefradil also suppressed total protein concentration in BALF, attenuated Evans blue extravasation, MPO activity, and NF-B activation in lung tissue. Furthermore, flunarizine, a widely prescripted antimigraine agent with potent inhibition on T-type channel, was also found to protect mice against lung injury. These data demonstrated that T-type calcium channel inhibitors may be beneficial for treating acute lung injury. The important role of T-type calcium channel in the acute lung injury is encouraged to be further investigated.
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http://dx.doi.org/10.1155/2020/3691701DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7671802PMC
November 2020

The Impact of Anlotinib on Brain Metastases of Non-Small Cell Lung Cancer: Post Hoc Analysis of a Phase III Randomized Control Trial (ALTER0303).

Oncologist 2020 05 20;25(5):e870-e874. Epub 2020 Feb 20.

Department of Thoracic Surgery and Oncology, the First Affiliated Hospital of Guangzhou Medical University, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou, People's Republic of China.

Background: Anlotinib has been shown to prolong progression-free survival (PFS) and overall survival (OS) for non-small cell lung cancer (NSCLC). Herein we sought to analyze the effect of anlotinib in managing brain metastases (BM) and its brain-associated toxicities.

Methods: The PFS and OS of anlotinib versus placebo in those with and without BM recorded at baseline were calculated and compared respectively. Time to brain progression (TTBP), a direct indicator of intracranial control, was also compared between anlotinib and placebo. All calculations were adjusted for confounding factors, including stage, histology, driver mutation type, and therapy history.

Results: A total of 437 patients were included; 97 cases were recorded with BM at baseline. For patients with BM at baseline, anlotinib was associated with longer PFS (hazard ratio [HR], 0.29; 95% confidence interval [CI], 0.15-0.56) and OS (HR, 0.72; 95% CI, 0.42-1.12), presenting similar extent of improvement in those without BM (PFS: HR, 0.33; 95% CI, 0.24-0.45; OS: HR, 0.67; 95% CI, 0.50-0.91). Specifically, the intracranial objective response rate was 14.3% and the disease control rate was 85.7% in patients with BM who were treated with anlotinib. Anlotinib was associated with longer TTBP (HR, 0.11; 95% CI, 0.03-0.41; p = .001) despite all confounders. Additionally, anlotinib was associated with more neural toxicities (18.4% vs. 8.4%) and psychological symptoms (49.3% vs. 35.7%) but not with infarction or cerebral hemorrhage.

Conclusion: Anlotinib can benefit patients with advanced NSCLC with BM and is highly potent in the management of intracranial lesions. Its special effect on BM and cerebral tissue merits further investigation. (ClinicalTrials.gov ID: NCT02388919).
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http://dx.doi.org/10.1634/theoncologist.2019-0838DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7216446PMC
May 2020

FOXC2 promotes epithelial-mesenchymal transition and cisplatin resistance of non-small cell lung cancer cells.

Cancer Chemother Pharmacol 2018 12 9;82(6):1049-1059. Epub 2018 Oct 9.

Department of Pharmacy, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang Road, Guangzhou, 510120, China.

Purpose: Platinum-based drugs, particularly cisplatin (DDP), are used in the treatment of non-small cell lung cancer (NSCLC). However, development of drug resistance remains the major therapeutic barrier in NSCLC.

Methods: The potential cisplatin resistance-related genes were identified from the global transcriptomes of cisplatin-resistant A549/DDP cells using microarray analysis. Gain- and loss-of-function assays were performed to analyze the effects of Forkhead Box Protein C2 (FOXC2) on the in vitro and in vivo sensitivity of NSCLC cells to cisplatin and its possible molecular mechanisms.

Results: Using global transcriptome analysis, we found that FOXC2 was one of the most upregulated molecules in A549/DDP cells compared with A549 cells. We further confirmed that the expression of FOXC2 was significantly increased in cisplatin-resistant NSCLC tissues. FOXC2 knockdown significantly increased the in vitro and in vivo sensitivity of A549/DDP cells to cisplatin, whereas overexpression of FOXC2 increased cisplatin resistance in cisplatin-sensitive NSCLC cells. Moreover, we found that FOXC2 promoted cisplatin resistance by induction of epithelial-mesenchymal transition (EMT) in NSCLC cells. Furthermore, FOXC2 activated the AKT/GSK3β signaling pathway, and then increased the protein expression of EMT-related transcription factor Snail. Inhibition of AKT or knockdown of Snail reversed FOXC2-induced EMT and cisplatin resistance of NSCLC cells.

Conclusion: FOXC2 enhanced cisplatin resistance of NSCLC cells through activating AKT/GSK3β/Snail/EMT signaling pathway, which may be a potential novel therapeutic target for overcoming drug resistance in human NSCLCs.
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http://dx.doi.org/10.1007/s00280-018-3697-2DOI Listing
December 2018

Preventive and Therapeutic Effects of Thymol in a Lipopolysaccharide-Induced Acute Lung Injury Mice Model.

Inflammation 2018 Feb;41(1):183-192

Department of Pharmacy, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.

Acute lung injury (ALI) is a life-threatening syndrome which causes a high mortality rate worldwide. In traditional medicine, lots of aromatic plants-such as some Thymus species-are used for treatment of various lung diseases including pertussis, bronchitis, and asthma. Thymol, one of the primary active constituent derived from Thymus vulgaris (thyme), has been reported to exhibit potent anti-microbial, anti-oxidant, and anti-inflammatory activities in vivo and in vitro. The present study aims to investigate the protective effects of thymol in lipopolysaccharide (LPS)-induced lung injury mice model. In LPS-challenged mice, treatment with thymol (100 mg/kg) before or after LPS challenge significantly improved pathological changes in lung tissues. Thymol also inhibited the LPS-induced inflammatory cells influx, TNF-α and IL-6 releases, and protein concentration in bronchoalveolar lavage fluid (BALF). Additionally, thymol markedly inhibited LPS-induced elevation of MDA and MPO levels, as well as reduction of SOD activity. Further study demonstrated that thymol effectively inhibited the NF-κB activation in the lung. Taken together, these results suggested that thymol might be useful in the therapy of acute lung injury.
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http://dx.doi.org/10.1007/s10753-017-0676-4DOI Listing
February 2018

Gevrey-smoothness of lower dimensional hyperbolic invariant tori for nearly integrable symplectic mappings.

Authors:
Shunjun Jiang

J Inequal Appl 2017 7;2017(1):39. Epub 2017 Feb 7.

College of Sciences, Nanjing Tech University, Nanjing, 210009 China.

This paper provides a normal form for a class of lower dimensional hyperbolic invariant tori of nearly integrable symplectic mappings with generating functions. We prove the persistence and the Gevrey-smoothness of the invariant tori under some conditions.
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http://dx.doi.org/10.1186/s13660-017-1307-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5306262PMC
February 2017