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Fig. 1.

The effect of sub-MIC of α-mangostin on the growth of Staphylococcus aureus planktonic cells. S. aureus SA113 was treated with α-mangostin, daptomycin, vancomycin, linezolid, and their synergistic combinations (½ × MIC), and the growth of planktonic cells was detected by optical density at 600 nm (OD600). The data presented was the average of three independent experiments (mean ± SD). MIC, minimum inhibitory concentration.
The effect of sub-MIC of α-mangostin on the growth of Staphylococcus aureus planktonic cells. S. aureus SA113 was treated with α-mangostin, daptomycin, vancomycin, linezolid, and their synergistic combinations (½ × MIC), and the growth of planktonic cells was detected by optical density at 600 nm (OD600). The data presented was the average of three independent experiments (mean ± SD). MIC, minimum inhibitory concentration.

Fig. 2.

The antibacterial effect of α-mangostin on the planktonic cells of Staphylococcus aureus. S. aureus SA113 during logarithmic growth phase was treated with α-mangostin, daptomycin, vancomycin, linezolid, and their synergistic combinations (4 × MIC), the remaining planktonic cells were enumerated. The data presented was the average of three independent experiments (mean ± SD). MIC, minimum inhibitory concentration.
The antibacterial effect of α-mangostin on the planktonic cells of Staphylococcus aureus. S. aureus SA113 during logarithmic growth phase was treated with α-mangostin, daptomycin, vancomycin, linezolid, and their synergistic combinations (4 × MIC), the remaining planktonic cells were enumerated. The data presented was the average of three independent experiments (mean ± SD). MIC, minimum inhibitory concentration.

Fig. 3.

Effect of different concentrations of α-mangostin on Staphylococcus aureus biofilms.
A) S. aureus SA113 and B) YUSA145 formed mature biofilms, then were treated with different concentrations of α-mangostin for 24 h. The remaining biofilm biomass was determined by crystal violet staining. The data presented was the average of three independent experiments (mean ± SD). Compared with control: *p < 0.05; **p < 0.01; ***p < 0.001; Student’s t-test. MIC – minimum inhibitory concentration
Effect of different concentrations of α-mangostin on Staphylococcus aureus biofilms. A) S. aureus SA113 and B) YUSA145 formed mature biofilms, then were treated with different concentrations of α-mangostin for 24 h. The remaining biofilm biomass was determined by crystal violet staining. The data presented was the average of three independent experiments (mean ± SD). Compared with control: *p < 0.05; **p < 0.01; ***p < 0.001; Student’s t-test. MIC – minimum inhibitory concentration

Fig. 4.

Schematic illustration of the SNPs in the sarT gene of the α-mangostin non-sensitive Staphylococcus aureus isolate. There were 35 SNPs located on both sides of the sarT gene, 10 SNPs in the sarT gene included one non-synonymous mutation (in red) and nine synonymous mutations.
Schematic illustration of the SNPs in the sarT gene of the α-mangostin non-sensitive Staphylococcus aureus isolate. There were 35 SNPs located on both sides of the sarT gene, 10 SNPs in the sarT gene included one non-synonymous mutation (in red) and nine synonymous mutations.

Fig. 5.

The different abundance proteins in-α-mangostin-treated Staphylococcus aureus isolate.
A) The molecular functions of different abundance proteins were classified by the GO analysis; B) different abundance proteins related to cell membrane synthesis and transport of biological process.
The different abundance proteins in-α-mangostin-treated Staphylococcus aureus isolate. A) The molecular functions of different abundance proteins were classified by the GO analysis; B) different abundance proteins related to cell membrane synthesis and transport of biological process.

Fig. 6.

Protein-protein interaction network of different abundance proteins in α-mangostin-treated Staphylococcus aureus isolate. The protein-protein interaction network of different abundance proteins was analyzed through STRING database.
Protein-protein interaction network of different abundance proteins in α-mangostin-treated Staphylococcus aureus isolate. The protein-protein interaction network of different abundance proteins was analyzed through STRING database.

Fig. 7.

The fluorescence intensity was significantly increased in α-mangostin-treated Staphylococcus aureus isolate. S. aureus SA113 was treated with α-mangostin, and staining with A) propidium iodide or B) bis(1,3-dibutylbarbituric acid) trimethine oxonol to evaluate the integrity of S. aureus cell membrane. The results were expressed in a relative fluorescence units. The data presented was the average of three independent experiments (mean ± SD).
The fluorescence intensity was significantly increased in α-mangostin-treated Staphylococcus aureus isolate. S. aureus SA113 was treated with α-mangostin, and staining with A) propidium iodide or B) bis(1,3-dibutylbarbituric acid) trimethine oxonol to evaluate the integrity of S. aureus cell membrane. The results were expressed in a relative fluorescence units. The data presented was the average of three independent experiments (mean ± SD).

Staphylococcus aureus susceptibility to α-mangostin.

S. aureus The MICs (μM) of α-mangostin
1.56 3.13 6.25 MIC50/MIC90
MSSA (n = 190) 16 163 11 3.13/3.13
MRSA (n = 138) 13 117   8 3.13/3.13
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Life Sciences, Microbiology and Virology