15 research outputs found
Neuronal Alterations and Antioxidant Status of Lipopolysaccharide Induced Neuronal damage in Mice: Eff icacy of Three Medicinal Plants
Background:
Several factors including neuroinflammation and oxidative stress formation contribute to the
progression and development of cognitive impairment. Lipopolysaccharide
(LPS) injection has been used as
non
-
transgenic mouse models for Alzheimer’s diseases (AD). Plant medicine has been proposed to be the
prospect in treatment/ management of neurodegenerative disease.
Aim:
The present study sought to evaluate the effect of
three medicinal plants (
Bacopa floribunda
(R.Br)Wettst
,
Scoparia dulcis
L and
Cordia millenii
Bak
.
) locally used for memory enhancement on neuronal histology and
antioxidant status against L
ipopolysaccharide induced neuronal damage in mice
.
Methods:
Forty
-
nine (49) BALB/c male mice were randomly grouped into seven (7) groups of 7 mice each. All
animals except in group I control (vehicle), were injected intraperitoneally (I.P.) with LPS (250 ÎĽg/kg) once,
after oral pre
-
treatment with plant extracts an
d control drugs for 7 days. Group II (untreated) received LPS only
(250 ÎĽg/kg) , group III received LPS + Sulindac Sulfide (SS, 4 mg/kg), group IV received LPS + Donepezil
(DPZ, 1 mg/kg) group V, VI, and VII received LPS + 200 mg/kg of plant extracts [
Sco
paria dulcis
(SD),
Bacopa floribunda
(BF), and
Cordia millenii
(CM)] respectively. After the experiment, histological analysis of
the hippocampus from the whole brain was carried out while the other brain tissue
s comprising frontal cortex
and
cerebellum we
re used for determination of biomarkers of antioxidant status such as catalase (CAT);
superoxide dismutase (SOD); malondialdehyde (MDA) and reduced glutathione (GSH).
Results:
Oral administration of LPS induced neuronal damage through cell death as eviden
ced by the
histological analysis and altered brain antioxidant status in mice. However, the plant extracts were able to
prevent such neuronal alterations and restored the antioxidant status when compared to the LPS induced
neuronal damage in mice.
Conclusi
on:
LPS induced neuroinflammation was prevented by the extracts of;
B. floribunda, S. dulcis
and
C.
millenni.
Neural damage was also prevented by the extracts. This activity could be attributed to their antioxidant
potential as evidenced from their inhibit
ory effect on MDA and increased CAT activity and GSH. Nevertheless,
other possible mechanisms of action against neuronal damage need to be assessed to further justify their use
traditionally in the treatment/management of neurodegenerative disease
Inhibition of neuroinflammation in BV2 microglia by the biflavonoid kolaviron is dependent on the Nrf2/ARE antioxidant protective mechanism
Kolaviron is a mixture of bioflavonoids found in the nut of the West African edible seed Garcinia kola, and it has been reported to exhibit a wide range of pharmacological activities. In this study, we investigated the effects of kolaviron in
neuroinflammation. The effects of kolaviron on the expression of nitric oxide/inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2)/cyclooxygenase-2, cellular reactive oxygen species (ROS) and the pro-inflammatory cytokines were examined in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. Molecular mechanisms of the effects of kolaviron on NF-B and Nrf2/ARE signalling pathways were analysed by immunoblotting, binding assay, and reporter assay. RNA interference was used to investigate the role of Nrf2 in the anti-inflammatory effect of kolaviron. Neuroprotective effect of kolaviron was
assessed in a BV2 microglia/HT22 hippocampal neuron co-culture. Kolaviron inhibited the protein levels of NO/iNOS, PGE2/COX-2, cellular ROS and the proinflammatory cytokines (TNFα and IL-6) in LPS-stimulated microglia. Further mechanistic studies showed that kolaviron inhibited neuroinflammation by inhibiting IB/NF-B signalling pathway in LPS-activated BV2 microglia. Kolaviron produced antioxidant effect in BV2 microglia by increasing HO-1 via the Nrf2/ antioxidant response element (ARE) pathway. RNAi experiments revealed that Nrf2 is need for the anti-inflammatory effect of kolaviron. Kolaviron protected HT22 neurons from neuroinflammation-induced toxicity. Kolaviron inhibits neuroinflammation through Nrf2-dependent mechanisms. This compound may therefore be beneficial in neuroinflammation-related neurodegenerative disorders
The gastroprotective effect of Memora nodosa roots against experimental gastric ulcer in mice
Original Article - ANALGESIC AND ANTI-INFLAMMATORY EFFECTS OF KOLAVIRON (A GARCINIA KOLA SEED EXTRACT)
Kolaviron is a defatted ethanol extract from the seeds of Garcinia
Kola. In the present study, the analgesic and anti-inflammatory
properties of Kolaviron is investigated using both thermal and chemical
models of pain assessment in mice and rats. Varying doses of Kolaviron
were given 30 minutes prior to the induction of abdominal constrictions
in mice and the determination of the mean tail immersion duration at
water bath temperature of 50.0 ± 10°C in mice. Kolaviron
exhibited dose-related anti-nociceptive properties against acetic acid
induced abdominal constrictions in mice: at 50mg/kg, it gave 28.92%
inhibition (P > 0.05) and at 200mg/kg it gave 55.49% inhibition (P
< 0.01). The compound also increased the mean tail immersion
duration at water bath temperature of 50.0 ± 1°C in mice