Bacterial Community Shift during the Startup of a Full-Scale Oxidation Ditch Treating Sewage

( Yajun Chen ),( Lin Ye ),( Fuzheng Zhao ),( Lin Xiao ),( Shupei Cheng ),( Xu-xiang Zhang ) 한국미생물 · 생명공학회 2017 Journal of microbiology and biotechnology Vol.27 No.1

The oxidation ditch (OD) is one of the most widely used processes for treating municipal wastewater. However, the microbial communities in the OD systems have not been well characterized, and little information about the shift of bacterial community during the startup process of the OD systems is available. In this study, we investigated the bacterial community changes during the startup period (over 100 days) of a full-scale OD. The results showed that the bacterial community dramatically changed during the startup period. Similar to the activated sludge samples in other studies, Proteobacteria (accounting for 26.3%-48.4%) was the most dominant bacterial phylum in the OD system, but its relative abundance declined nearly 40% during the startup process. It was also found that Planctomycetes proliferated greatly (from 4.79% to 13.5%) and finally replaced Bacteroidetes as the second abundant phylum in the OD system. Specifically, some bacteria affiliated with genus Flavobacterium exhibited remarkable decreasing trends, whereas bacterial species belonging to the OD1 candidate division and Saprospiraceae family were found to increase during the startup process. Despite of the bacterial community shift, the organic matter, nitrogen, and phosphorus in the effluent were always in low concentrations, suggesting the functional redundancy of the bacterial community. Moreover, by comparing with the bacterial community in other municipal wastewater treatment bioreactors, some potentially novel bacterial species were found to be present in the OD system. Collectively, this study improved our understandings of the bacterial community structure and microbial ecology during the startup of a full-scale wastewater treatment bioreactor.

The protection of Rhein lysinate to liver in diabetic mice induced by high-fat diet and streptozotocin

Yajun Lin,Gang Hu,Kai-Ji Li,Yu-Fang Zhao,Jie Wei,Yongzhan Zhen 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.5

Rhein lysinate (RHL) is the salt of lysine andrhein and the objective of this study was to investigate theprotection of RHL to liver in diabetic mice. The model oftype 2 diabetes was established by high-fat diet andstreptozotocin treatment. Malondialdehyde, superoxidedismutase (SOD) and glutathione peroxidase (GSH-Px)were measured using a spectrophotometer. Inflammatoryfactors (TNF-a and IL-6) and related proteins (ERK1/2 andSREBP-1c) were analyzed by Western blot. Tissue profilewas determined by hematoxylin and eosin staining andaccumulation of fat was examined by Nile red staining. The results indicated that plasma glucose levels of type 2diabetic mice were over 13.9 mM. Compared with modelgroup, plasma glucose levels were decreased, howeverinsulin levels were increased in RHL (25 and 50 mg/kg)-treated group. Elevated plasma triglyceride and cholesterolwere also markedly attenuated after RHL treatment. Theactivities of SOD and GSH-Px of livers were increasedafter RHL treatment. Livers of RHL-treated mice had morenormal structure and less steatosis than that of diabeticmice. Moreover, RHL decreased the expression of TNF-aand IL-6 and the phosphorylation of SREBP-1c and ERK1/2. In conclusion, RHL has a noticeable hepatic protectionin diabetic mice.

Rhein lysinate inhibits monocyte adhesion to human umbilical vein endothelial cells by blocking p38 signaling pathway

Yajun Lin,Yongzhan Zhen,Jiang Liu,Jie Wei,Ping Tu,Gang Hu 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.11

The objective of this study was to investigate theeffect of rhein lysinate (RHL) on monocyte adhesion and itsmechanism. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assay was used to determine thegrowth inhibition by drugs. The monocyte chemoattractantprotein (MCP)-1 levels were assayed using MCP-1 ELISA. The expression of proteins was detected by Western blottinganalysis. The results indicated that RHL inhibited monocyteadhesion in a dose- and time-dependent manner. RHL(\20 lmol/L) and lipopolysaccharide (LPS) had no effecton viability of human umbilical vein endothelial cells. Therefore, 20 lmol/L RHL was selected for this study. RHLinhibited secretion ofMCP-1 induced by LPS and expressionof intercellular adhesion molecule (ICAM)-1 and vascularcell adhesion molecule (VCAM)-1. In the meantime, bothRHL and p38 inhibitor (SB203580) inhibited phosphorylationof p38 and mitogen-activated protein kinase-activatedprotein kinase-2 (MAPKAPK-2) and transcription andexpression of ICAM-1 and VCAM-1. In conclusion, RHLinhibits the transcription and expression of ICAM-1 andVCAM-1 by the p38/MAPKAPK-2 signaling pathway, andthe effect ofRHLon transcription and expression of ICAM-1and VCAM-1 is similar to p38 inhibitor. RHL could be aprophylactic drug for atherosclerosis.

Long non-coding RNA RP11-6O2.4 indicates poor prognosis and suppresses cell cycle progression through the p38-MAPK signaling pathway in gastric cancer

Yang Feng,Zhiming Fu,Yajun Luo,Wang Tan,Zilin Liu,Pengcheng Ye,Fei Lu,Wanping Xiang,Linghan Tang,Lin Yao,Mengyun Song,Qingmei Huang,Yilun Liu,Jiangwei Xiao 대한독성 유전단백체 학회 2019 Molecular & cellular toxicology Vol.15 No.3

Backgrounds: The role of long non-coding RNAs (lncRNA) in gastric cancer (GC) has been highlighted in studies conducted over the past decade. However, the potential clinical value and the mechanisms of action of RP11-6O2.4 in GC have not been thoroughly elucidated to date. The specific aim of the present study was to assess RP11-6O2.4 and to explore its role in human GC. Methods: Quantitative real-time polymerase chain reaction (qPCR) was performed to analyze the expression levels of RP11-6O2.4 in GC tissues, paired adjacent noncancerous tissues (ANTs) and GC cell lines. In addition, the correlation between RP11-6O2.4 expression and the clinical characteristics and prognosis of patients with GC was statistically analyzed. The effects of RP11- 6O2.4 on the GC cell cycle transformation through the p38-MAPK signaling pathway were explored by flow cytometry, qPCR and Western blot analysis after treatment with SB203580, a p38MAPK specific inhibitor, in vitro. Results: The expression levels of RP11-6O2.4 in GC tissues were significantly lower than the paired ANTs (P<0.05). In addition, RP11-6O2.4 expression was significantly lower in cases with older age, longer maximum tumor diameter, higher ASA grade and deeper invasive depth (P<0.05). RP11-6O2.4 expression was significantly higher in cases with well/middle differentiation than poor/no differentiation; higher in cases without lymph node metastasis than in lymph node metastasis; and higher in cases in stage Ⅰ/Ⅱ than in stage Ⅲ/Ⅳ. An in vitro assay showed that RP11-6O2.4 induced G0/ G1 phase cell cycle arrest, likely by regulating the p38- MAPK signaling pathway. Conclusion: The above mentioned data suggested that RP11-6O2.4 was a tumor-suppressor gene in GC. RP11- 6O2.4 might play an important role in the cell cycle transformation by regulating the p38-MAPK signaling pathway, thereby representing a specific biomarker and a potential molecular target for the treatment of GC.

Rhein lysinate decreases inflammation and adipose infiltration in KK/HlJ diabetic mice with non-alcoholic fatty liver disease

Jie Wei,Yong-Zhan Zhen,Ju Cui,Fa-Lin He,Tao Shen,Gang Hu,Xiao-Hong Ren,Yajun Lin 대한약학회 2016 Archives of Pharmacal Research Vol.39 No.7

The objective of this study was to investigate the protective effects of rhein lysinate (RHL) on the liver. Mice were divided into four groups: C57BL/J control, the KK/HlJ diabetic model, and 25 and 50 mg/kg/day RHLtreated KK/HlJ groups. The KK/HlJ diabetic mouse model was made by injecting STZ and feeding mice diabetic food. At 16 weeks, mice were sacrificed and their livers were harvested. The results indicated that compared with the C57BL/J control group, the body weights, liver weights and liver weight-to-body weight ratio were increased in KK/HlJ diabetic mice; however, these values were decreased following treatment with RHL. Compared with the C57BL/J control, KK/HlJ diabetic mice had a significantly lower level of SOD and GSH-px in their livers, but had a significantly higher level of MDA. However, these effects were ameliorated by RHL. Hepatic adipose infiltration was observed in KK/HlJ mice, but not in C57BL/J mice. RHL decreased the incidence of hepatic adipose infiltration and significantly decreased the expression of TNF-a, IL-6, NF-jB, SREBP-1c, and Fas, as well as the phosphorylation of NF-jB in the liver. In conclusion, RHL can improve hepatic function by decreasing hepatic adipose infiltration and the expression of inflammatory factors.