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| 1 | TLR9 agonist enhances radiofrequency ablation-induced CTL responses, leading to the potent inhibition of primary tumor growth and lung metastasis显示文摘Radiofrequency ablation(RFA)is the most common approach to thermal ablation for cancer therapy.Unfortunately,its efficacy is limited by incomplete ablation,and further optimization of RFA is required.Here,we demonstrate that incubation at 65°C triggers more EG7 tumor cell death by necrosis than treatment at 45°C,and the 65°C-treated cells are more effective at inducing antigen-specific CD8^(+)cytotoxic T lymphocyte(CTL)responses after injection in mice than the 45°C-treated ones.Dendritic cells(DCs)that phagocytose 65°C-treated EG7 cells become mature with upregulated MHCII and CD80 expression and are capable of efficiently inducing effector CTLs in mouse tumor models.RFA(65°C)therapy of EG7 tumors induces large areas of tumor necrosis and stimulates CTL responses.This leads to complete regression of small(~100 mm^(3))tumors but fails to suppress the growth of larger(~350 mm^(3))tumors.The administration of the Toll-like receptor-9(TLR9)agonist unmethylated cytosine-phosphorothioate-guanine oligonucleotide(CpG)to DCs phagocytosing 65°C-treated EG7 cells enhances the expression of MHCII and CD40 on DCs as well as DC-induced stimulation of CTL responses.Importantly,the intratumoral administration of CpG following RFA also increases the frequencies of tumor-associated immunogenic CD11b−CD11c^(+)CD103^(+)DC2 and CD11b+F4/80+MHCII+M1 macrophages and increases CD4^(+)and CD8^(+)T-cell tumor infiltration,leading to enhanced CD4^(+)T cell-dependent CTL responses and potent inhibition of primary RFA-treated or distant untreated tumor growth as well as tumor lung metastasis in mice bearing larger tumors.Overall,our data indicate that CpG administration,which enhances RFA-induced CTL responses and ultimately potentiates the inhibition of primary tumor growth and lung metastasis,is a promising strategy for improving RFA treatment,which may assist in optimizing this important cancer therapy. | Aizhang Xu Lifeng Zhang Jingying Yuan Fatma Babikr Andrew Freywald Rajni Chibbar Michael Moser Wenjun Zhang Bing Zhang Zhaoying Fu Jim Xiang | 2019 | Cellular & Molecular Immunology2019，16，10： | 3 |
| 2 | Effects of chronic peripheral pretreatment with an angiotensin II type-1 receptor blocker on apoptosis-related molecules in rats with cerebral ischemia/reperfusion injury显示文摘Chronic systemic treatment with blockers of angiotensin II type-1(AT1) receptors inhibits ischemia-induced apoptosis and reduces ischemic neuronal damage.However,the molecular mechanisms of AT1 receptor blockers in modulating neuronal apoptosis remain poorly understood.Pretreatment with irbesartan significantly suppressed cell apoptosis at 1-7 days following cerebral ischemia/reperfusion,increased levels of brain-derived neurotrophic factor,and elevated the ratios of Bcl-2/Bax and phosphorylated cyclic adenosine monophosphate response element-binding protein(pCREB)/CREB in the ischemic cortex at 1 day after reperfusion,as well as suppressing caspase-3 activation.Cerebral ischemia increased the mRNA expression of AT1 and AT2 receptors in the ischemic cortex,whereas irbesartan blocked this increase in AT1 expression but potentiated the expression of AT2.Therefore,this AT1 receptor blocker was neuroprotective by increasing the ratios of Bcl-2/Bax and pCREB/CREB,increasing brain-derived neurotrophic factor levels,inhibiting caspase-3 activation,and modulating AT receptor expression. | Jingping Shi Jingde Dong Jie Lu Yingdong Zhang | 2010 | Neural Regeneration Research2010，5，15： | 2 |
| 3 | Molecular Pathway of Psoralidin-Induced Apoptosis in HepG2 Cell Line显示文摘Objective: To test the role of psoralidin in human liver cancer HepG2 cells in vitro. Methods: Cell viability was assessed by methylthiazolyldiphenyl-tetrazolum bromide assay and apoptotic cells were labeled by annexin V then sorted by flow cytometry. Protein expressions of caspase-3, caspase-8, caspase-9, Bax, Bid, Bcl-2, Bcl-xL and p53 were examined by western blot while activity of caspase-3,-8 and -9 were also determined. Results: Psoralidin reduces cell viability greatly in a time dependent manner(64%, 40%, 21%, 12% at 2, 6, 24 and 48 h treatment with 64 μmol/L psoralidin respectively) and up-regulates activities of caspase-3,-8 and-9 in a concentration dependent manner(between 4 to 64 μmol/L). Psoralidin also increases the expression of pro-apoptosis genes Bax, Bid and p53 while decreases the expression of pro-survival genes Bcl-2 and Bcl-xL, both in a concentration dependent manner between 4 and 64 μmol/L(P<0.05 at 16 and 64 μmol/L). Caspase-3 inhibitor(Ac-DEVD-CHO at concentrations between 10 to 20 μmol/L), p53 inhibitor(pifithrin-α at 5 μmol/L) and cyclosporin A can attenuate the apoptotic effect of psoralidin. Conclusion: The cytotoxic role of psoralidin might work through both intrinsic and extrinsic apoptotic pathway. | YU Bin WANG An-hong ZHOU Kun CHAI Li-juan LIU Lu | 2019 | Chinese Journal of Integrative Medicine2019，25，10： | 0 |
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