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There is a good saying: "The butt determines the head", simply put, the "position" people are in determines "how to think and how to do"
.
Maybe everyone wants to say, this is just a life proverb, as the brain of the supreme commander, how can it allow other organs to challenge authority?
From a biological and medical point of view, the ass is really impossible, but the gut can! This is the current hot research direction in the scientific research community: microbiota-gut-brain axis (MGBA), that is, the intestinal flora may affect brain function and behavior
through neurological, immune and endocrine pathways.
Parkinson's disease (PD) is a common neurodegenerative disease, and studies have shown that one of the main causes of PD is an imbalance in the gut flora, for which probiotic preparations may have therapeutic effects, but the mechanism and pathway are unknown
.
Recently, Tian Fengwei's team from China published an article entitled "Neuroprotective Effects of Bifidobacterium breve CCFM1067 in MPTP-Induced Mouse Models of Parkinson's Disease" in a well-known journal of nutrition ", the research paper proves that probiotic B.
breve CCFM1067 can prevent or treat PD by modulating MGBA, and may be used as an oral supplement
for PD treatment in the future.
Doi: _mstmutation="1" _istranslated="1"> researchers selected 40 6-week-old male C57BL/6 mice and randomly divided them into four groups of 10: control group, MPTP group, L-DOPA group and B.
Breve CCFM1067 group
.
It should be noted that MPTP is the abbreviation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which can be used in the construction of Parkinson's disease models in experimental animals; L-DOPA, short for levodopa, is a prodrug of dopamine (DA) that is currently thought to improve Parkinson's disease symptoms; B.
breve CCFM1067 is a species of
Bifidobacterium breve.
The experiment lasted for a total of 41 days, and on days 33-37, mice in other groups were subjected to daily MPTP intervention except the control group, and L-DOPA mice in the L-DOPA group were orally L-DOPA on days 33~41; B.
Breve CCFM1067 group mice orally B.
breve CCFM1067
。 All mice were weighed, feces collected weekly, and further experiments
such as behavioral testing, mRNA expression, etc.
were performed.
In this study, a total of four behavioral tests were carried out to test the motor function of mice, namely Pole Test (PT), narrow-beam test (NBT), rotarod test (RTR), and open field test (OFT).
。 The results showed that compared with the control group, the mice in the MPTP group showed obvious movement disorders, and their motor agility, balance and coordination decreased, while those in the B.
Treatment with breve CCFM1067 significantly reduces MPTP-induced dyskinesia
.
Bifidobacterium breve CCFM1067 alleviates MPTP-induced motor dysfunction
in mice, and dopamine (DA) in the brain works in tandem with the glutamate system to control the body's motor and cognitive functions
。 The synthesis of DA is influenced by the rate-limiting enzyme tyrosine hydroxylase (TH), and motor symptoms of PD occur
when TH levels fall below a certain threshold 。 Histopathological staining results showed that the intake of B.
breve CCFM1067 effectively inhibited the decrease of TH expression in the substantia nigra (SN), while the levels of neurotransmitters such as DA, DOPAC and 5-HT in the striatum of PD mice were significantly increased, and the expression of neurotrophic factors BDNF and GDNF was restored, suggesting that B.
breve CCFM1067 can reduce MPTP-induced neuropathological changes and glial activation, and has a neuroprotective effect on PD mice, which partly explains the intrinsic reason
for the improvement in mouse behavior.
B.
breve CCFM1067 can mitigate MPTP-induced neuropathological changes and glial activation
What are the possible mechanisms by which CCFM1067 exerts a neuroprotective role in PD mice?
In addition to the neurotrophic factors mentioned above, reactive oxygen species and inflammatory responses are also key factors in the development of
PD.
The results showed that through B.
breve CCFM1067 treatment enhances the antioxidant capacity of the central nervous system, suggesting B.
breve CCFM1067 helps PD mice reduce peroxide toxicity and relieve oxidative stress
.
In addition, the study found that B.
breve CCFM1067 inhibited pro-inflammatory gene expression and protein expression in PD mice, reduced brain and intestinal inflammation, enhanced anti-inflammatory ability, and it is worth pointing out that the increase in short-chain fatty acids may be one of the reasons why B.
breve CCFM1067 has an anti-inflammatory effect on the intestine or brain of
PD mice.
Next, the researchers examined the mRNA expression of three key cytokines (TNF-α, IL-1β, and IL-6) in the striatum and colon of mice, and the data showed that the disruption of the intestinal barrier due to dysbacteriosis of the gut led to the leakage of pro-inflammatory cytokines, which in turn led to systemic inflammation
.
However, B.
breve CCFM1067 treatment reduces intestinal inflammation and prevents the development of
PD, which is achieved by improving the health of the intestinal barrier, preventing leakage of inflammatory molecules, and reducing inflammation in the brains of PD mice.
The results of fecal microbiota analysis showed that the intervention of B.
breve CCFM1067 could act on MPTP-induced intestinal microbiota imbalance, inhibit the number of pathogenic bacteria (Shigella) in PD mice, while increasing the number of beneficial bacteria (Bifidobacterium and Ackermania), i.
e.
, the protective effect of B.
breve CCFM1067 may be mediated by restoring normal flora, while the side emphasized The importance of
dysbiosis in PD progression.
B.
The effect of breve CCFM1067 treatment on MPTP-induced intestinal microbial function in mice with PD may be mediated by microbial metabolites, as shown above, this study suggests
Probiotic B.
breve CCFM1067 has neuroprotective effects on dopaminergic neurons in MPTP-induced mouse models of PD, and can improve MPTP-induced dyskinesia, dopaminergic neuron death, and neurotransmitter reduction
in mice.
A possible mechanism for its neuroprotective role in PD mice is to reduce glial overactivation, oxidative stress damage, inflammatory response, and intestinal dysbacteriosis
by increasing neurotrophic factor and short-chain fatty acid levels.
I hope that one day in the future, probiotics can truly become an effective adjunct to the prevention and treatment of Parkinson's disease!
References: Tiantian Li, Chuanqi Chu, Leilei Yu, et al.
Neuroprotective Effects of Bifidobacterium breve CCFM1067 in MPTP-Induced Mouse Models of Parkinson’s Disease.
Nutuients.
2022, 14, 4678.
Source: | Biovalley
Editor | Alaska Treasure
