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Articles by Jie Song
Total Records ( 5 ) for Jie Song
  Na Li , Jie Song , Liang Kong , Shao-Heng Li , Ya-Nan Jiao , Yu-Hui Yan , Ying-Jia Yao , Ya-Kun Meng , Xiao-Fei Li , Miao-Miao Tong , Nan Zhang , Kai Kang , Ting-Guo Kang and Jing-Xian Yang
  Background and Objective: Mechanical trauma injury is caused by some external force which does harm to the vasculature, tissues and neighboring neuronal cells. This injury is a serious insult to neuronal cells which may release lactate dehydrogenase as the characteristics of cell damage. The release of inflammatory cytokines in injury cells is a normal immune response but the over expression of some pro-inflammatory cytokines such as interleukin-6 and tumor necrosis factor-α are detrimental to wound recovery. Suppression of pro-inflammatory cytokines is beneficial to alleviate mechanical trauma injury-induced cell damage. The present study aims to establish the mechanical trauma injury model in vitro and investigate the protective effect of 2,3,5,4’-tetrahydroxystilbene-2-O-glucoside on this model and its mechanism. Materials and Methods: The SH-SY5Y cells were used to establish the mechanical trauma injury model in vitro by scratching out the monolayer and generating an area devoid of cells. Then, the extent of cell damage of the model was measured by lactate dehydrogenase content determination and 12 h was confirmed as the key time point to explore 2,3,5,4’-tetrahydroxystilbene-2-O-glucoside concentration given. The cell viability was measured by cell counting kit-8 to determine the optimal concentration of drug administration. The extent of cell damage was detected by immunofluorescence analysis to observe whether 2,3,5,4’-tetrahydroxystilbene-2-O-glucoside can protect the integrity of the cell structure TUNEL staining was used to detect whether it can decrease cell apoptosis. Finally, Tested the inflammatory cytokine levels (interleukin-6, interleukin-10 and tumor necrosis factor-α) by enzyme-linked immunosorbent assays, reverse transcription-polymerase chain reaction and western blotting to clarify the mechanism of cytoprotection. Data were assessed by the SPSS version 13.0. Results: The 2,3,5, 4’-tetrahydroxystilbene-2-O-glucoside increased viability of SH-SY5Y cells and the migrative ability, protected the integrity of cell structure, reduced apoptosis, decreased pro-inflammatory cytokine levels (interleukin-6 and tumor necrosis factor-α) and increased anti-inflammatory cytokine level (interleukin-10) in mechanical trauma injury-induced SH-SY5Y cell model. Conclusion: These studies demonstrate that 2,3,5, 4’-tetrahydroxystilbene-2-O-glucoside relieves the mechanical trauma injury-induced damage in SH-SY5Y cells by attenuating the levels of inflammatory responses. This might help us to further understand the pharmacological role of 2,3,5,4’-tetrahydroxystilbene-2-O-glucoside in anti-inflammation and neuroprotection in the neural cells.
  Na Li , Jia-Bo Wang , Yan-Ling Zhao , Lin Zhang , Xi-Bo Ma , Xiao-Fei Li , Jie Song , Xin Yang , Xiao-He Xiao , Jie Tian and Ting-Guo Kang
  Background: Hepatocytes damage is sometimes closely related to oxidative stress and reactive oxygen species which are the major contributors to lipopolysaccharide-induced liver injury. Emodin, the active natural product in rhubarb of hydroxyanthraquinone skeleton, has been reported of protective activity to liver tissue, whose mechanism is generally thought of antioxidation based on chemical reaction or indirect evidence. There is no visualized evidence proved the reactive oxygen species scavenging effect of emodin in vivo. Materials and Methods: The dynamic reactive oxygen species luminescent signal in mice injured by bacillus calmette guerin and lipopolysaccharide was monitored by using the optical molecular imaging approach. Results: The elevations of serum alanine aminotransferase and aspartate transaminase activities in bacillus calmette guerin/lipopolysaccharide-injured mice were reversed by emodin, indicating the protection of emodin to hepatocytes. And emodin significantly and dose-dependently attenuated the reactive oxygen species luminescent signal elicited by bacillus calmette guerin/lipopolysaccharide, indicating visually the in vivo reactive oxygen species scavenging effect of emodin. In addition, emodin significantly and dose-dependently elevated the activity of superoxide dismutase, content of reduced glutathione and total antioxidant capacity and meanwhile decreased the contents of hydrogen peroxide, lipid peroxides and malondialdehyde in livers of bacillus calmette guerin/lipopolysaccharide-injured mice. It could be attributed to the anti-oxidative effect of emodin which helps to maintain the reactive oxygen species balance in vivo. Conclusion: Emodin can protect liver against bacillus calmette guerin/lipopolysaccharide-induced injury and the mechanism includes reactive oxygen species scavenging effect and anti-lipid peroxidation at least.
  Peng Wang , Teng-Fei Long , Li-Ping Wang and Jie Song
  Background and Objective: Epidemiological studies have shown admiring protective roles of phytochemicals on peripheral nervous system, while the prevalent use of hypotensive drugs directly impacts normal functioning of the nervous system. Hence, the present study was assessed the synergistic role of Asiatic Acid (AA) and Madecassic Acid (MA) against the antioxidant deficit induced by the metoprolol tartrate. Materials and Methods: Wistar male rats (150 mg kg1) were divided into 4 groups. Group 1 as control with no treatment, group 2 rats with metoprolol tartrate (150 mg kg1/day, orally), group 3 rats pre-treated with AA (50 mg kg1, IP) and MA (30 mg kg1, IP) for 2 weeks prior to metoprolol tartrate and group 4 with AA and MA combined as drug control for 28 days. Blood pressure (BP), heart rate (HR) and other antioxidant parameters were monitored and the blood samples were collected for endocrine and biochemistry analysis. Results: Metoprolol administration demonstrated a significant reduction in body weight, systolic BP, heart rate and food intake, while the levels of lipid peroxidation was increased significantly compared to control rats. Also, a significant decrease (p<0.01) in the antioxidant levels such as; SOD, catalase, glutathione peroxidase, reduced glutathione were evidenced in metoprolol group. On the other hand, the neuronal markers enzyme acetylcholinesterase were reduced while the activity of Nitric Oxide Synthase (NOS), Cytochrome P450 Reductase (CPR) and Carbonic anhydrase were increased in metoprolol group compared to control. However, rats received AA and MA pre-treatment elicited the improved antioxidant enzymes with restored physiological parameters, food intake and reduced the marker enzymes activity. Conclusion: The results of present study demonstrated the protective role of AA and MA against antioxidant deficit induced by the metoprolol tartrate by improving the physiological functions.
  Feng Tang , Hong-Lin Ren , Yun-Ming Xu , De-Ying Zou , Nan-Nan Liu , Yan-Song Li , Yu Zhou , Jie Song , Zhao-Hui Li , Yuan-Yuan Zhang , Shi-Ying Lu and Zeng-Shan Liu
  Brucellosis is a zoonosis which is caused by Brucella species and pruduces severe economic losses and a public health problem. At present, the diagonsis of Brucella infection mainly depends on serological tests to detect antibodies in sera and the animal brucellosis is prevented via vaccine. In this study, the kinetics and cross-reactivity of antibodies in sera were evaluated in Small Tail Han sheep (Ovis arie) infected with a virulent field strain of Brucella melitensis (BmF) and ones inoculated with a vaccine strain S2 of B. suis under laboratory conditions. Serum samples were collected at 0, 3, 7, 14, 21, 30, 40, 44, 50, 60 and 75 days post-challenge (dpc) and were analyzed by Rose Bengal Plate Agglutination Test (RBPT) and indirect Enzyme-Linked Immunosorbent Assay (iELISA). Sera samples of BmF-challenged and S2-challenged sheep groups at 40, 44, 50, 60 and 75 dpc were tested positive to Brucella by the RBPT, nevertheless the earliest positive reaction results were observed in sera at 21 dpc by iELISA. The virulent field strain BmF initiated a higher level of antibody titer than vaccine strain S2 without statistic significant difference (p>0.05). The cross-reactivities with the virulent and the vaccine stains were confirmed in serum antibodies between the BmF-challenged group and the S2-challenged group. The results indicated that the serodiagnosis is hard to distinguish the brucella-infected sheep from the vaccine-inoculated sheep. Diagnosis methods of identifying between the healthy and the infected animals need to further be studied in future.
  Lei Li , Wei Deng , Jie Song , Wei Ding , Qun- Fei Zhao , Chao Peng , Wei- Wen Song , Gong -Li Tang and Wen Liu
  Saframycin A (SFM-A), produced by Streptomyces lavendulae NRRL 11002, belongs to the tetrahydroisoquinoline family of antibiotics, and its core is structurally similar to the core of ecteinascidin 743, which is a highly potent antitumor drug isolated from a marine tunicate. In this study, the biosynthetic gene cluster for SFM-A was cloned and localized to a 62-kb contiguous DNA region. Sequence analysis revealed 30 genes that constitute the SFM-A gene cluster, encoding an unusual nonribosomal peptide synthetase (NRPS) system and tailoring enzymes and regulatory and resistance proteins. The results of substrate prediction and in vitro characterization of the adenylation specificities of this NRPS system support the hypothesis that the last module acts in an iterative manner to form a tetrapeptidyl intermediate and that the colinearity rule does not apply. Although this mechanism is different from those proposed for the SFM-A analogs SFM-Mx1 and safracin B (SAC-B), based on the high similarity of these systems, it is likely they share a common mechanism of biosynthesis as we describe here. Construction of the biosynthetic pathway of SFM-Y3, an aminated SFM-A, was achieved in the SAC-B producer (Pseudomonas fluorescens). These findings not only shed new insight on tetrahydroisoquinoline biosynthesis but also demonstrate the feasibility of engineering microorganisms to generate structurally more complex and biologically more active analogs by combinatorial biosynthesis.
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