1.EXPERIMENTAL RESEARCH ON THE ANTIFATIGUE EFFECT OF FLAMMULINA VELUTIPES
Jing WEN ; Wen CHEN ; Jin WANG ; Zhonglian JIN ;
Acta Nutrimenta Sinica 1956;0(01):-
The present paper reports a systematic research of the antifatigue effect of Flammulina velutipes. The antifatigue effect was judged by the examination of serum lactate dchydrogenase activity, level of blood lactic acid, serum urea nitrogen, muscle and liver glycogen,The experiments indicated that feeding Flammulina velutipes to mice for several days the lactate dehydrogenase activity, muscle and liver glycogeu levels were significantly higher than that of the control. After exercise, the levels of blood lactate and serum urea nitrogen were significantly lower than those of control. After exercise, the recovery rate of lactic acid was much faster than that of control.From the above results, we concluded the Flammulina velutipes may have significant effect on the capability of adaptation to heavy exercise and prevention or elimination of fatigue after exercise.
2.VEGF-B antibody and interleukin-22 fusion protein ameliorates diabetic nephropathy through inhibiting lipid accumulation and inflammatory responses.
Yilan SHEN ; Wei CHEN ; Lei HAN ; Qi BIAN ; Jiajun FAN ; Zhonglian CAO ; Xin JIN ; Tao DING ; Zongshu XIAN ; Zhiyong GUO ; Wei ZHANG ; Dianwen JU ; Xiaobin MEI
Acta Pharmaceutica Sinica B 2021;11(1):127-142
Diabetic nephropathy (DN) is considered the primary causes of end-stage renal disease (ESRD) and is related to abnormal glycolipid metabolism, hemodynamic abnormalities, oxidative stress and chronic inflammation. Antagonism of vascular endothelial growth factor B (VEGF-B) could efficiently ameliorate DN by reducing renal lipotoxicity. However, this pharmacological strategy is far from satisfactory, as it ignores numerous pathogenic factors, including anomalous reactive oxygen species (ROS) generation and inflammatory responses. We found that the upregulation of VEGF-B and downregulation of interleukin-22 (IL-22) among DN patients were significantly associated with the progression of DN. Thus, we hypothesized that a combination of a VEGF-B antibody and IL-22 could protect against DN not only by regulating glycolipid metabolism but also by reducing the accumulation of inflammation and ROS. To meet these challenges, a novel anti-VEGFB/IL22 fusion protein was developed, and its therapeutic effects on DN were further studied. We found that the anti-VEGFB/IL22 fusion protein reduced renal lipid accumulation by inhibiting the expression of fatty acid transport proteins and ameliorated inflammatory responses