Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
 
Articles by Ting-Guo Kang
Total Records ( 2 ) for Ting-Guo Kang
  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.
 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility