The glioma cells U251 and U87 MG at the logarithmic phase were divided into control group （0 μmol·L^－1 AdipoRon） and 20， 40， 60， 80，and 100 μmol·L^－1 AdipoRon groups. The proliferation rates of the cells in various groups at 24， 48，and 72 h were detected by CCK-8 assay.The U251 and U87 MG cells were divided into control group （0 μmol·L^－1 AdipoRon） and 40， 60， and 80 μmol·L^－1 AdipoRon groups.The clone formation rates of the cells in various groups were detected by clone formation assay， the scratch healing rates of the cells in various groups were detected by scratch healing experiment， the apoptotic rates and the percentages of the cells at different cell cycles were detected by flow cytometry， and the expression levels of AMP-dependent protein kinase （AMPK） and phosphorylated AMPK （p-AMPK） proteins in the cells in various groups were detected by Western blotting method.The U251 cells were divided into shNC control group（given no treatment） and shNC group（given 40 μmol·L^－1 Adiporon）， AdipoR1 knockdown group （given 40 μmol·L^－1 Adiporon， knockdown AdipoR1）， AdipoR2 knockdown group （given 40 μmol·L^－1 Adiporon， knockdown AdipoR2） and AdipoR1+AdipoR2 co-knockdown group （given 40 μmol·L^－1 Adiporon， knockdown AdipoR1 and AdipoR2）. The proliferation rates of the U251 cells in various groups were detected by CCK-8 assay， and the expression levels of AdiopR1 and AdiopR2 mRNA in the U251 cells were detected by real-time fluorescence quantitative PCR （RT-qPCR）method.

Compared with control group， the proliferation rates of the U251 and U87 MG cells in different concentrations of AdipoRon groups were decreased at 24， 48 and 72 h （P<0.05 or P<0.01）. Compared with control group， the clone formation rates of the U251 and U87 MG cells in 40， 60，and 80 μmol·L^－1 AdipoRon groups were decreased （P<0.01）. Compared with control group， the scratch healing rates of the U251 and U87 MG cells in 40， 60，and 80 μmol·L^－1 AdipoRon groups were decreased after 48 h treatment （P<0.01）. Compared with control group， the apoptotic rates of the U251 cells in 60 and 80 μmol·L^－1 AdipoRon groups and the U87 MG cells in 80 μmol·L^－1 AdipoRon group were increased （P<0.01）； the percentages of the U251 and U87 MG cells at G₀/G₁ phase in 40， 60， and 80 μmol·L^－1 AdipoRon groups were increased （P<0.01）. Compared with control group， the expression levels of p-AMPK protein in the U251 cells in 60 and 80 μmol·L^－1 Adiporon groups were increased （P<0.01），and the expression levels of p-AMPK protein in the U87 MG cells in 40， 60， and 80 μmol·L^－1 Adiporon group were increased （P<0.05 or P<0.01）. Compared with shNC control group， the expression level of AdipoR1 mRNA in the U251 cells in AdipoR1 knockdown group was decreased （P<0.01）， and the expression level of AdipoR2 mRNA in the U251 cells in AdipoR2 knockdown group was decreased （P<0.01）. Compared with shNC control group， after treated with of 40 μmol·L^－1 Adiporon， the proliferation rates of the U251 cells in AdipoR1 knockdown group， AdipoR2 knockdown group， and AdipoR1+AdipoR2 co-knockdown group were increased （P<0.05 or P<0.01）.

Adiporon can inhibit the proliferation， migration and apoptosis of the glioma cells and block the cell cycle at G₀/G₁ phase， and its mechanism may be that adiporon interacts with the adiponectin receptors AdipoR1 and AdipoR2 to promote the AMPK phosphorylation， thus affecting the biological behaviors of the glioma cells.