1045
Original Paper
Cell Physiol Biochem 2011;28:1045-1050
Accepted: July 25, 2011
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Baicalein Suppresses the SOS Response System
of Staphylococcus Aureus Induced by
Ciprofloxacin
Qing Peng
1
, Shuqin Zhou
2
, Fen Yao
1
, Bing Hou
3
, Yuanchun Huang
4
,
Dexing Hua
5
, Yanshan Zheng
1
and Yuanshu Qian
1
1
Pharmacology Department, Shantou University Medical College, Shantou, Guangdong,
2
Zhujiang
Hospital, Southern medical University, Guangzhou, Guangdong,
3
Clinical Laboratory of Dermatosis
Hospital, Shantou, Guangdong,
4
Clinical Laboratory of First Affiliated Hospital, Shantou University Medical
College, Shantou, Guangdong
5
Clinical Laboratory of Yuebei Hospital, Shaoguan, Guangdong
Y. S. Qian
Pharmacology Department, Shantou University Medical College
Shantou, Guangdong, 515041 (R. P. China)
Tel. + 86 754 8890 0432, Fax +86 754 8855 7562
E-Mail beckypeng@yahoo.cn
Key Words
Bacailein • SOS response • Staphylococcus aureus •
Ciprofloxacin
Abstract
Numerous antibiotics can induce an SOS repair
system in bacteria that leads to antibiotic-resistant
mutation of the bacterium. Therefore, searching for
drugs that can prevent the SOS response and thus
improve the long-term viability of some antibiotics is
important. In this study, we aimed to detect the
suppressive effects of baicalein on the SOS system
and rifampin-resistant mutation in Staphylococcus
aureus. We determined the reactive oxygen species
(ROS) formation and intracellular ATP level in S.
aureus with baicalein treatment to investigate the
mechanisms involved in its effects on the SOS system.
The results showed that baicalein was a potent
inhibitor of the expression of the SOS genes RecA,
LexA and SACOL1400. The rifampin-resistant
mutation rate of S. aureus induced by ciprofloxacin
was significantly reduced after treatment with
baicalein. Treatment with baicalein led to a significant
decrease in intracellular reactive oxygen species
(ROS) formation and ATP level. Our findings indicate
that baicalein may be an SOS-response inhibitor in S.
aureus through inhibiting ROS formation and ATP
production and may be used to prevent excessive
mutation induced by antibiotics.
Introduction
Staphylococcus aureus infection can be difficult
to treat because of multidrug resistance and the organism’s
remarkable ability to persist in the host. Persistence and
the evolution of resistance may be related to several
complex regulatory networks such as the SOS response,
which is essential in bacterial mutations. SOS system uses
the RecA protein, which is stimulated by single-stranded
DNA, to inactivate the LexA repressor and induce the
response.
In addition to the fluoroquinolones [1-3], other
antibiotics, such as rifampin [4], aminoglycosides [5], and
β-lactams [5, 6], can induce the SOS response and cause
mutations resulting in multidrug resistance. Therefore,