The objective of this study was to evaluate anti-obesity effects
of kimchi microbial community (KMC) on obesity and
gut microbiota using a high fat diet-induced mouse model
compared to effects of a single strain. Administration of KMC
decreased body weight, adipose tissue, and liver weight gains.
Relative content of Muribaculaceae in the gut of the KMCtreated
group was higher than that in the high-fat diet (HFD)
group whereas relative contents of Akkermansiaceae, Coriobacteriaceae,
and Erysipelotrichaceae were lower in KMCtreated
group. Metabolic profile of blood was found to change
differently according to the administration of KMC and a
single strain of Lactobacillus plantarum. Serum metabolites
significantly increased in the HFD group but decreased in
the KMC-treated group included arachidic acid, stearic acid,
fumaric acid, and glucose, suggesting that the administration
of KMC could influence energy metabolism. The main genus
in KMC was not detected in guts of mice in KMC-treated
group. Since the use of KMC has advantages in terms of
safety, it has potential to improve gut microbial community
for obese people.
San-Ying Wang , Jing Zhang , Xiao-Gang Xu , Hui-Li Su , Wen-Min Xing , Zhong-Shan Zhang , Wei-Hua Jin , Ji-Huan Dai , Ya-Zhen Wang , Xin-Yue He , Chuan Sun , Jing Yan , Gen-Xiang Mao
J. Microbiol. 2020;58(8):716-723. Published online June 10, 2020
Human cytomegalovirus (hCMV) is a ubiquitous herpesvirus,
which results in the establishment of a latent infection that
persists throughout the life of the host and can be reactivated
when the immunity is low. Currently, there is no vaccine for
hCMV infection, and the licensed antiviral drugs mainly target
the viral enzymes and have obvious adverse reactions.
Thus, it is important to search for compounds with antihCMV
properties. The present study aimed to investigate the
suppressive effects of piceatannol on hCMV Towne strain
infection and the putative underlying mechanisms using human
diploid fibroblast WI-38 cells. Piceatannol supplementation
prevented the lytic changes induced by hCMV infection
in WI-38 cells. Furthermore, piceatannol suppressed the
expression of hCMV immediate-early (IE) and early (E) proteins
as well as the replication of hCMV DNA in a dose-dependent
manner. Moreover, hCMV-induced cellular senescence
was suppressed by piceatannol, as shown by a decline
in the senescence-associated β-galactosidase (SA-β-Gal) activity
and decreased production of intracellular reactive oxygen
species (ROS). p16INK4a, a major senescence-associated
molecule, was dramatically elevated by current hCMV infection
that was attenuated by pre-incubation with piceatannol
in a dose-dependent manner. These results demonstrated
that piceatannol suppressed the hCMV infection via
inhibition of the activation of p16INK4a and cellular senescence
induced by hCMV. Together, these findings indicate piceatannol
as a novel and potent anti-hCMV agent with the potential
to be developed as an effective treatment for chronic
hCMV infection.