Notice of RetractionThe Anti-Damage Ability of the Bamboo Leaves Extract

Notice of Retraction

After careful and considered review of the content of this paper by a duly constituted expert committee, this paper has been found to be in violation of IEEE´s Publication Principles.

We hereby retract the content of this paper. Reasonable effort should be made to remove all past references to this paper.

The presenting author of this paper has the option to appeal this decision by contacting TPII@ieee.org.

Objective In this paper, extracts of bamboo leaves, Phyllostachys praecox (BLE) have been selected to explore their effect on cell proliferation, antioxidant capacity, anti-DNA damage and anti-inflammation injury ability in vitro. Methods DPPH free radical scavenging test and ultra-weak chemiluminescence assay were applied to measure the antioxidant capacity of the bamboo leaves extract; MTT assay was used to detect the cell proliferation effect of the extracts and PM_2.5; Comet assay was applied to the DNA strand breakage detection of the H₂O₂, induced RAW264.7 and anti-DNA damage of BLE. Western blot method was used to detect the expression of NF-kB in A549 cell. Results (1) BLE had the abilities of removing DPPH free radicals and IC₅₀ was 7.02mg/L, which was lower than that of ascorbic acid (2.43mg/L). (2) BLE decrease and delay the DNA damage significantly in CuSO₄-Phen-Vc-H₂O₂-DNA reaction of ultra-weak chemiluminescence system. (3) The tail DNA content was decrease by BLE significantly on H₂O₂-induced RAW264.7. (4) BLE showed little cytotoxicity for A549 cell and can resist the changes in cell viability that caused by different concentrations of PM_2.5. (5) 100mg/L of PM_2.5 could cause a significantly high expression of NF-kB in A549 nuclear, but 40mg/L BLE could resist the activation of NF-kB stimulated by PM_2.5. Conclusion BLE have the potential ability of DPPH free radical sca- enging, anti-DNA strand breakage by H₂O₂-induced, anti-inhibitive effect on cell proliferation induced by the PM_2.5 and anti-inflammation by decreasing the activation of NF-kB stimulated by PM25.