Endophytic fungi harbored in Panax notoginseng: diversity and potential as biological control agents against host plant pathogens of root-rot disease

You-Kun Zheng,Cui-Ping Miao,Hua-Hong Chen,Fang-Fang Huang,Yu-Mei Xia,You-Wei Chen,Li-Xing Zhao 고려인삼학회 2017 Journal of Ginseng Research Vol.41 No.3

Background: Endophytic fungi play an important role in balancing the ecosystem and boosting host growth. In the present study, we investigated the endophytic fungal diversity of healthy Panax notoginseng and evaluated its potential antimicrobial activity against five major phytopathogens causing rootrot of P. notoginseng. Methods: A culture-dependent technique, combining morphological and molecular methods, was used to analyze endophytic fungal diversity. A double-layer agar technique was used to challenge the phytopathogens of P. notoginseng. Results: A total of 89 fungi were obtained from the roots, stems, leaves, and seeds of P. notoginseng, and 41 isolates representing different morphotypes were selected for taxonomic characterization. The fungal isolates belonged to Ascomycota (96.6%) and Zygomycota (3.4%). All isolates were classified to 23 genera and an unknown taxon belonging to Sordariomycetes. The number of isolates obtained from different tissues ranged from 12 to 42 for leaves and roots, respectively. The selected endophytic fungal isolates were challenged by the root-rot pathogens Alternaria panax, Fusarium oxysporum, Fusarium solani, Phoma herbarum, and Mycocentrospora acerina. Twenty-six of the 41 isolates (63.4%) exhibited activity against at least one of the pathogens tested. Conclusion: Our results suggested that P. notoginseng harbors diversified endophytic fungi that would provide a basis for the identification of new bioactive compounds, and for effective biocontrol of notoginseng root rot.

Endophytic fungi harbored in Panax notoginseng: diversity and potential as biological control agents against host plant pathogens of root-rot disease

Zheng, You-Kun,Miao, Cui-Ping,Chen, Hua-Hong,Huang, Fang-Fang,Xia, Yu-Mei,Chen, You-Wei,Zhao, Li-Xing The Korean Society of Ginseng 2017 Journal of Ginseng Research Vol.41 No.3

Background: Endophytic fungi play an important role in balancing the ecosystem and boosting host growth. In the present study, we investigated the endophytic fungal diversity of healthy Panax notoginseng and evaluated its potential antimicrobial activity against five major phytopathogens causing root-rot of P. notoginseng. Methods: A culture-dependent technique, combining morphological and molecular methods, was used to analyze endophytic fungal diversity. A double-layer agar technique was used to challenge the phytopathogens of P. notoginseng. Results: A total of 89 fungi were obtained from the roots, stems, leaves, and seeds of P. notoginseng, and 41 isolates representing different morphotypes were selected for taxonomic characterization. The fungal isolates belonged to Ascomycota (96.6%) and Zygomycota (3.4%). All isolates were classified to 23 genera and an unknown taxon belonging to Sordariomycetes. The number of isolates obtained from different tissues ranged from 12 to 42 for leaves and roots, respectively. The selected endophytic fungal isolates were challenged by the root-rot pathogens Alternaria panax, Fusarium oxysporum, Fusarium solani, Phoma herbarum, and Mycocentrospora acerina. Twenty-six of the 41 isolates (63.4%) exhibited activity against at least one of the pathogens tested. Conclusion: Our results suggested that P. notoginseng harbors diversified endophytic fungi that would provide a basis for the identification of new bioactive compounds, and for effective biocontrol of notoginseng root rot.

A novel pattern recognition protein of the Chinese oak silkmoth, Antheraea pernyi, is involved in the pro-PO activating system

Xia Lu Wan,Zhang Jing Hai,Ying Chen,You Lei Ma,Wen Jun Zou,Guo Yuan Ding,Wei Li,Ming Yi Zhao,Chun Fu Wu 생화학분자생물학회(구 한국생화학분자생물학회) 2013 BMB Reports Vol.46 No.7

Down-regulation of Phosphoglucose Isomerase/Autocrine Motility Factor Enhances Gensenoside Rh2 Pharmacological Action on Leukemia KG1α Cells

You, Zhi-Mei,Zhao, Liang,Xia, Jing,Wei, Qiang,Liu, Yu-Min,Liu, Xiao-Yan,Chen, Di-Long,Li, Jing Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.3

Aims and Background: Ginsenoside Rh2, which exerts the potent anticancer action both in vitro and in vivo, is one of the most well characterized ginsenosides extracted from ginseng. Although its effects on cancer are significant, the underlying mechanisms remain unknown. In this study, we sought to elucidate possible links between ginsenoside Rh2 and phosphoglucose isomerase/autocrine motility factor (PGI/AMF). Methods: $KG1{\alpha}$, a leukemia cell line highly expressing PGI/AMF was assessed by western blot analysis and reverse transcription- PCR (RT-PCR) assay after transfection of a small interfering (si)-RNA to silence PGI/AMF. The effect of PGI/AMF on proliferation was measured by typan blue assay and antibody array. A cell counting kit (CCK)-8 and flow cytometry (FCM) were adopted to investigate the effects of Rh2 on PGI/AMF. The relationships between PGI/AMF and Rh2 associated with Akt, mTOR, Raptor, Rag were detected by western blot analysis. Results: KG1${\alpha}$ cells expressed PGI/AMF and its down-regulation significantly inhibited proliferation. The antibody array indicated that the probable mechanism was reduced expression of PARP, State1, SAPK/JNK and Erk1/2, while those of PRAS40 and p38 were up-regulated. Silencing of PGI/AMF enhanced the sensibility of $KG1{\alpha}$ to Rh2 by suppressing the expression of mTOR, Raptor and Akt. Conclusion: These results suggested that ginsenoside Rh2 suppressed the proliferation of $KG1{\alpha}$, the same as down-regulation of PGI/AMF. Down-regulation of PGI/AMF enhanced the pharmacological effects of ginsenoside Rh2 on KG1${\alpha}$ by reducing Akt/mTOR signaling.

Geographic Variations of Stroke Incidence in Chinese Communities: An 18-Year Prospective Cohort Study from 1997 to 2015

Fan Xia,Xuexin Yu,Yunke Li,Yuqi Chen,Wei Zhang,Chao You,Xin Hu 대한뇌졸중학회 2020 Journal of stroke Vol.22 No.3

Background and Purpose As a leading cause of disability and death in China, stroke as well as its epidemiologic features have gained increasing attention. Prior studies, however, have overgeneralized the north-to-south gradient in China. Whether the differences exist across urban and rural areas remains unexplored. This study therefore aims to investigate the north-to-south gradient in stroke incidence across urban and rural China. Methods The present prospective cohort study analyzed data from the China Health and Nutrition Survey 1997 to 2015. By including 16,917 individuals from diverse social contexts, we calculated the age-standardized incidence of stroke across regions and the age-adjusted risk ratio (aRR). Cox proportional hazards models with time-varying covariates were employed to analyze variations in incident stroke. Results During the follow-up, age-standardized incidence of stroke ranged from 4.17 per 1,000 person-years (95% confidence interval [CI], 3.38 to 4.96) in the north region to 1.95 (95% CI, 1.60 to 2.30) in the south region (aRR, 2.04; 95% CI, 1.58 to 2.64; P<0.001). The north-to-south gradient of stroke incidence was observed only in rural areas, but not in urban areas. Hierarchical modelling analyses further indicated that the regional differences could be mostly explained by the disparities in the prevalence of hypertension. Conclusions The present study extends the current evidence on the north-to-south gradient by demonstrating that the difference varied across urban and rural China. Our findings highlight the importance of hypertension management as the measure for alleviating regional differences in stroke incidence.

Poster Session:PS 0234 ; Gastroenterology : Effect of Mir-34a in Regulating Steatosis by Targeting PPARa Expression in NAFLD

( Jie Xia Ding ),( Meng Li ),( Xi Jin ),( Shao Hua Chen ),( Chao Hui Yu ),( You Ming Li ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1

Background: The association between altered expression of miR-34a and pathophysiological features of nonalcoholic fatty liver disease (NAFLD) and whether there is a connection between susceptibility to NAFLD has not been completely clarifi ed. Methods: The vitro model was established by culturing L02 cells with a high concentration of free fatty acid (FFA) and the vivo model was established by feeding C57BL/6 mice with HFD. To determine the effects of miR-34a, cultured L02 cells transfected with miR-34a inhibitor and C57BL/6 mice injected with miR-34a inhibitor through vein tail were analysed for the level of PPARaand the metabolic sensor AMPK. In functional experiments, TG content and steatosis degree were measured by TG assay kit, HE and Oil Red O staining. Results: miR-34a expression is signifi cantly upregulated in steatosis-induced hepatocytes and in liver tissues of HFD fed mice. The upregulation of miR-34a resulted in the downregulation of hepatic peroxisome proliferator-activated receptor-a(PPARa), the direct target of miR-34a. Moreover, the action of miRNA-34a on PPAR-a depends on the presence of a single miRNA-34a binding site. Silencing miR-34a led to an initial increase the level of PPARaand the targets of PPARa, including CPT1, CPT2, SLC27A4, SLC27A1 and ACBD3. Activation of the central metabolic sensor AMPK was also increased. In functional experiments, miR-34a inihibitor suppressed cell and mice liver TG content and improve steatosis degree. Furthermore, inhibition of PPARa expression aggravated hepatocellular steatosis in vitro models. Conclusions: NAFLD is associated with altered hepatic miR-34a expression. Decreased expression of miR-34a potentially contributes to altered lipid metabolism implicated in the pathogenesis of NAFLD. These results suggest that regulating it`s target PPARa by down-regulation of miR-34a levels may be a therapeutic strategy against NAFLD.

Poster Session:PS 0235 ; Gastroenterology : Hadha Plays a Role of Double-Edged Sword in Hepatic Steatosis and Cell Injury in Nonalcoholic Fatty Liver Disease

( Jie Xia Ding ),( Meng Li ),( Xing Yong Wan ),( Xi Jin ),( Shao Hua Chen ),( Chao Hui Yu ),( You Ming Li ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1

Background: The mechanisms of pathogenesis underlying nonalcoholic fatty liver disease (NAFLD) remain unclear at present and the depth study of HADHA in the development of NAFLD has never been investigated. Methods: The NAFLD cell model was established by treating L02 cells with free fatty acid (FFA) overload. Small interfering RNA (siRNA) was used to knock down HADHA level. The expression of HADHA and key enzymes associated with fatty acid beta- oxidation in L02 cells were determined by q-PCR. Key protein associated in energy metabolism, endoplasmic reticulum(ER) stress and infl ammatory were determined by western blotting. ATP, hydroperoxide (H2O2), catalase (CAT) and mitochondrial membrane potential (MMP) were measured. The prediction of HADHA upstream regulation of miRNA was carried out and luciferase reporter assays were implemented to validate the prediction. Results: After culturing L02 cells by FFA for 48h, we detect the increased protein level of HADHA. HADHA knockdown in L02 cells resulted in an increased of lipid accumulation and downregulation of gene expression involved in fatty acid beta-oxidation, including PPARa, ACOX1, CPT2, EHHADH, ECHS1, HADHB and HADH. Additionally, administering HADHA siRNA exhibited improvement of oxidative stress, embodied in decreased level of H2O2 and MDA, meanwhile, increased levels of ATP, CAT and MMP. Furthermore, HADHA knockdown demonstrated weakened AMPK pathway, activation of MAPK and MKK3 pathway, and improve ER stress by downregulation of C/EBPa and C/EBPß. Moreover, HADHA was regulated directly by upstream gene of miR-124. Conclusions: Our results show that HADHA may plays a role of double-edged sword in hepatic steatosis and cell injury in NAFLD, and provide a new insight into the pathogenic mechanisms of NAFLD, may becoming a potential new therapeutic target for NAFLD.

Human Papillomavirus Infection and Prognostic Predictors in Patients with Oropharyngeal Squamous Cell Carcinoma

Huang, Hui,Zhang, Bin,Chen, Wen,Zhou, Shuang-Mei,Zhang, Yong-Xia,Gao, Li,Xu, Zhen-Gang,Qiao, You-Lin,Tang, Ping-Zhang Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.3

This study focused on infection rates and subtypes of human papillomavirus (HPV) in patients with oropharyngeal squamous cell carcinoma (OSCC), and the relationship between HPV status and prognosis of the disease. We evaluated sixty-six OSCC patients who met the enrollment criteria during the period from January 1999 to December 2009. The presence or absence of oncogenic HPV types in tumors was determined using the SPF10 LiPA25 assay. Overall survival (OS) and disease specific survival (DSS) for HPV positive and HPV negative patients were estimated using Kaplan-Meier analysis. The Cox regression model was applied for multivariate analysis. HPV-DNA was detected in 11(16.7%) of all specimens. Among them, 7 were type HPV-16, while other types were HPV-16/11, HPV-35, HPV-58/52, and HPV-33/52/54. Patients with HPV positive tumors were more likely to be female, non-smokers and non-drinkers (p=0.002, 0.001 and 0.001, respectively). After a median follow-up of 24.5 months, patients with HPV positive tumors had significantly better overall survival (HR=0.106[95%CI=0.014-0.787], p=0.016,) and disease specific survival (HR=0.121[95%CI=0.016-0.906], p=0.030). Patients with HPV positive OSCC have significantly better prognosis than patients with HPV negative tumors. HPV infection is an independent prognostic factor.

Apatinib Combined with Local Irradiation Leads to Systemic Tumor Control via Reversal of Immunosuppressive Tumor Microenvironment in Lung Cancer

Li-jun Liang,Chen-xi Hu,Yi-xuan Wen,Xiao-wei Geng,Ting Chen,Guo-qing Gu,Lei Wang,You-you Xia,Yong Liu,Jia-yan Fei,Jie Dong,Feng-hua Zhao,Yiliyar Ahongjiang,Kai-yuan Hui,Xiao-dong Jiang 대한암학회 2020 Cancer Research and Treatment Vol.52 No.2

Purpose This study aimed to investigate the potential systemic antitumor effects of stereotactic ablative radiotherapy (SABR) and apatinib (a novel vascular endothelial growth factor receptor 2 inhibitor) via reversing the immunosuppressive tumor microenvironment for lung carcinoma. Materials and Methods Lewis lung cancer cells were injected into C57BL/6 mice in the left hindlimb (primary tumor; irradiated) and in the right flank (secondary tumor; nonirradiated). When both tumors grew to the touchable size, mice were randomly divided into eight treatment groups. These groups received normal saline or three distinct doses of apatinib (50 mg/kg, 150 mg/kg, and 200 mg/kg) daily for 7 days, in combination with a single dose of 15 Gy radiotherapy or not to the primary tumor. The further tumor growth/regression of mice were followed and observed. Results For the single 15 Gy modality, tumor growth delay could only be observed at the primary tumor. When combining SABR and apatinib 200 mg/kg, significant retardation of both primary and secondary tumor growth could be observed, indicated an abscopal effect was induced. Mechanism analysis suggested that programmed death-ligand 1 expression increased with SABR was counteract by additional apatinib therapy. Furthermore, when apatinib was combined with SABR, the composition of immune cells could be changed. More importantly, this two-pronged approach evoked tumor antigen–specific immune responses and the mice were resistant to another tumor rechallenge, finally, long-term survival was improved. Conclusion Our results suggested that the tumor microenvironment could be managed with apatinib, which was effective in eliciting an abscopal effect induced by SABR.

Ginsenoside Rg1 Induces Apoptosis through Inhibition of the EpoR-Mediated JAK2/STAT5 Signalling Pathway in the TF-1/Epo Human Leukemia Cell Line

Li, Jing,Wei, Qiang,Zuo, Guo-Wei,Xia, Jing,You, Zhi-Mei,Li, Chun-Li,Chen, Di-Long Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.6

Ginsenoside Rg1 is one effective anticancer and antioxidant constituent of total saponins of Panax ginseng (TSPG), which has been shown to have various pharmacological effects. Our previous study demonstrated that Rg1 had anti-tumor activity in K562 leukemia cells. The aim of this study was designed to investigate whether Rg1 could induce apoptosis in TF-1/Epo cells and further to explore the underlying molecular mechanisms. Here we found that Rg1 could inhibit TF-1/Epo cell proliferation and induce cell apoptosis in vitro in a concentration and time dependent manner. It also suppressed the expression of EpoR on the surface membrane and inhibited JAK2/STAT5 pathway activity. Rg1 induced up-regulation of Bax, cleaved caspase-3 and C-PAPR protein and down-regulation of Bcl-2 and AG490, a JAK2 specific inhibitor, could enhance the effects of Rg1. Our studies showed that EpoR-mediated JAK2/STAT5 signaling played a key role in Rg1-induced apoptosis in TF-1/Epo cells. These results may provide new insights of Rg1 protective roles in the prevention a nd treatment of leukemia.