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Liu et al. Low antioxidant status of patients with CNSI

reported before. In conclusion, our findings suggest neuroprotectant against oxidative stress injury.
[27]
that there were low serum levels of UA, bilirubin and Moreover, increasing evidences suggested that
albumin in patients with CNSI. bilirubin also possessed multiple biological activities,
including potential immunomodulatory properties.
[28]
The mechanisms of CNS damage during meningitis Our results supported the finding that serum bilirubin
have not been conclusively identified. Increasing levels in CNSI were lower than the control group, in
evidence shows a massive production of ROS and spite of there being no apparent difference when
RNS could lead to significant collateral damage in compared with multiple sclerosis (MS). Furthermore,
pneumococcal meningitis, because of their toxic gender differences also existed, and we found that
actions, such as lipid peroxidation, DNA strand women also had lower mean serum bilirubin values
breakage and production of inflammatory cytokines. when compared with men.
Therefore, a potential use of oxidative inhibitors
as an adjunctive treatment could be beneficial in Otherwise, some researchers demonstrated that serum
treating meningitis. [18] Our work showed that patients albumin, specifically block echovirus by inhibiting the
with CNSI had low serum UA, Tbil, Ibil and albumin uncoating step in the virus replication cycle. That is to
levels. The notion is that oxidative damage plays a say that in man, echovirus infection may be modulated
crucial role in CNSI, which may be because of the low by serum albumin. [29]
antioxidant status.
Imbalanced metabolism and excess free radical
UA is a natural antioxidant in the blood and brain, generation could cause oxidative stress, which
which has been shown that exogenous administration has been defined as a principle pathological cause
of urate is protective in experimental bacterial of neurodegenerative disorders, such as MS,
[23]
meningitis. UA is capable of scavenging free Parkinson’s disease. Therefore, it could be
[19]
[30]
radicals and chelating transitional metal ions by favorable for increasing antioxidant levels, such as
preventing peroxynitrite induced protein nitrosylation, UA, bilirubin and albumin levels in CNSI, which should
lipid and protein peroxidation, and inactivation of not focus only on anti-infective therapy, but also on the
tetrahydrobiopterin. Low levels of UA are detrimental antioxidant effects.
[20]
to neurons, while high levels of UA contribute to
neuroprotection. [21,22] In conclusion, low serum UA, bilirubin and albumin
levels in CNSI patients were found in our study, the
Our study showed that serum levels of UA in patients reason may be due to exhaustion of antioxidant
with CNSI were lower, therefore, increasing in UA capacity. An imbalance between oxidant and
concentration has been suggested as one of the antioxidant activities will result in the development of
possible mechanisms as a replacement therapy. intracranial inflammation and destruction of neurons.
Generally speaking, serum UA levels are highly sex These findings may increase our understanding of
and age dependent. In this study, we further divided pathophysiology of CNSI. Therefore, to enhance
each group into female and male subgroups, [23] we antioxidant power and keep oxidative stress and
found that in all groups, men had higher serum UA antioxidant in balance may be beneficial to patients
levels than women which is consistent with previous with CNSI, that is to say, improving the clinical and
studies. [17,24] laboratory results in CNSI, by elevating serum UA,
bilirubin and albumin could be considered.
Bilirubin, the end product of heme metabolism,
is formed from biliverdin. As the products of In the future, we plan to measure the antioxidant levels
Hemeoxygenase (HO)-catalyzed heme breakdown, in cerebrospinal fluid (CSF) of CNSI patients, and we
it has an essential cerebroprotective role. [11,12] There may compare the antioxidant status of blood and CSF
are two major forms of HO, existing HO-1 and HO-2. in these patients.
It is generally accepted that the elevated HO-1 levels
represent an attempt to restore redox homeostasis Financial support and sponsorship
and to down-modulate inflammation. HO-2, Nil.
[25]
the constitutively active isoform, has an essential
cerebroprotective role against seizure-induced loss of Conflicts of interest
endothelial vasodilator function in newborn piglets. There are no conflicts of interest.
[26]
Some observations suggested that bilirubin, as a
potent antioxidant, could reduce cerebrovascular Patient consent
complications in the seizures of newborn babies. Informed consent was obtained from all individual
[12]
Some scholars provided that bilirubin could be as participants included in the study.
266 Neuroimmunology and Neuroinflammation ¦ Volume 3 ¦ December 15, 2016