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Neuroprotective effects

A neuroprotective effect simply means a protective effect on the nervous system. Usually, it is meant mainly the ability of substances to protect brain cells (neurons) from dying, such as ischemia, irritation, or chemical poisoning. Neurons are among the body cells to the most gentle. When they stop the oxygen supply they die very quickly. They are very sensitive to heavy metals and react to other poisons much earlier than normal cells of the human body. Therefore, the effect of alcohol on the brain is noticed after the first blow, while we have to devour it for several years to exert its influence on the liver. Therefore, when heavy metals are poisoned, the nervous symptoms are the first. The brain can be damaged by a lack of sleep or permanent stress , in which neurons can not be constantly activated. Neuron, who is constantly active, gets tired and dies more easily. This causes an alarm of the brain cells, called glia. (It's the glie, not the glie, the glial cell in the singular.) The brain works in the human body in complete isolation, behind a blood-brain barrier that does not allow the normal immune cells to cross. The role of immune cells in the brain is replaced by specialized macrophages, called microglia . (Again, it's the microglie, not the microglia, the singular cell of the cell, the cell of the microglie.) Microglia plays a role in the brain, but it still remembers that it comes from the immune cells , and when it jumps, it can make a nice gauntlet. The microglie is still on guard, and if any bacteria, virus, or other pathogens are trying to get into the brain, they're going to get their fighting gear and you get inflammation of the brain. Microglia does not count on eating and fetching, causing problems for neurons. When you eat and have a hangover , the microglie thinks if the poor drunk neurons get rabies or other viral diseases. And they immediately begin to investigate, arrest and proclaim martial law, causing you headaches and often in a good attempt to kill more neurons than alcohol itself. Frankly, if you get poisoned your neurons properly, such as lead or mercury, no miraculous herb is safe. But when you just irritate or advise, they can adaptogens with an anti-inflammatory effect to explain your microglia that the situation is not so serious as to require inflammation. An entirely analogous situation occurs in brain ischemia, for example, stroke. This effect of adaptogenes is terribly called "soothing effect on microglia". In rare cases, the microglie itself loses consciousness and begins to attack without reason its own neurons - it is called autoimmunity and it is one of the mechanisms of aging. Adaptogens with a soothing effect on microglia in these conditions help to slow the progression of the disease. Of course, it would be a great simplification to put an equation between neuroprotective effect and soothing effect on microglia. The neuroprotective effect of herbs is achieved by many other mechanisms - for example, by speeding up detoxification, by improving blood supply (by ischemia), by preventing apoptosis (when the neuron itself suspects of viral infection or malignancy) or simply by improving nutrition and vitamin intake.

From the neuroprotective effects, each adapogen with an effect on immunity can be considered. And blue already knows that plants with an anti-inflammatory effect and, as a matter of fact, pain as "pancakes" among adaptogens are preferentially pushed. The anti-inflammatory effects also include the ginseng modelogenetic adaptogen, which underwent extensive research that demonstrated its neuroprotective capabilities.

Neuroprotective effects of ginseng

Ginseng contains substances that have the ability to calm the microglia and act in the brain exactly as I suggested in the introductory paragraph. See studies Zhang2008pgg , Li2007peg , Wu2007deg , Lin2007gra , Liao2002neg and others. The effects can be attributed to individual panaxosides .

  • Wu2007deg shows that gssd. Rb 2 , Rd , Rg 1 and Re have a strong inhibitory effect on the production of TNF-α microglia-activated lipopolysaccharides. Gssd Rg 1 and Re also blocked microglia production of NO. Their inhibitory effect on NF-κB transcription factor and other elements of the stress microglia activation cascade (MAPK1, MAPK3, MAPK8) has been confirmed.
  • In experiments on neuronal cultures, it has demonstrated a protective effect by limiting the inflammation reaction of the microglia and by reducing the production of NO and prostaglandin E2 induced by the addition of bacterial lipopolysaccharides ( Lin2007gra ).
  • Pxsd. Rb 1 and Rg 1 had a protective effect on spinal neurons in vitro ( Liao2002neg ).
  • Bae2006grr illustrates the protective effect of ginseng in ischemic stroke with gssd suppressive effect. Rg 3 and Rh 2 to detrimentally activate the microglia. Lipopolysaccharide-activated or interferon-γ activated mice blocked Rh 2 expression of inducible NO synthase (NOS2 gene) and production of NO with IC 50 = 17 μM by blocking the binding of transcription factor AP-1 to DNA. This also reduced the expression of cycloxygenase 2 (the PTGS2 gene) and the inflammatory cytokines TNF-α and IL-1β. Rh 2 further enhanced the expression of IL-10 inhibiting inflammation and facilitated the binding of CREB transcription factor to DNA. There was no Rh 2 effect on the binding of NF-κB transcription factor. Effect of gssd. Rg 3 was similar to Rh 2 , but much weaker.
  • Gssd Rg 2 prevents neuronal death, protects memory and other brain functions in the ischemia / reperfusion model ( Zhang2008pgg ), and protects neurons against glutamate damage ( Li2007peg ) in vitro.
  • Ginsenoside Rd prevented damage to dopaminergic neurons due to inflammatory activation of microglia by bacterial lipopolysaccharides. ( Lin2007gra )
  • Ginsenoside Rg 3 , which is primarily produced by ginseng on red ginseng , reduces the expression of cytokines in inflammatory activated microglia and inhibits the binding of NF-κB transcription factor to the respective DNA binding sites, resulting in increased survival of neuronal cells in vitro. Ginsenoside Rg 3 also almost completely blocked the expression of NOS2 (iNOS) and increased the expression of MSRA (macrophage scavenger receptor type A). ( Joo2008pin )
  • Ginseng polysaccharides protect the brain against autoimmune damage in an experimental mouse model ( Hwang2011app )
  • Nie2006pep - ginseng panaxynol and panaxydol protect brain neurons subjected to chemical stress before dying.

Neuroprotective effects of LBP polysaccharides contained in the pulp.

Publications on the neuroprotective effect of the polysaccharides of the sculpture came from a group of scientists at the University of Hong Kong, especially from in vitro experiments, at a time when I was intensively engaged in the subject. Previous treatment with the LBP aqueous extract has preserved rat cortex neurons from the Aβ toxicity (amyloid beta is a protein that appears to be the major constituent of plaque in the brain of Alzheimer's disease ) ( Yu2005nea ). In one of the rare in vivo studies, the effect of LBP on glaucoma caused by high intraocular pressure was investigated. Rats harvested by the LBP extract showed a significant decrease in the number of retinal ganglion neurons. However, the intraocular pressure did not change ( Chan2007nel ). It is virtually certain that over time, the neuroprotective effect of the clergyman will be devoted to other researchers, in which the reader refers to primary sources.

Other neuroprotective adaptogens

Neuroprotective effects have been found in many adapogenic and medicinal plants. From specific publications, I draw attention to:

  • Recent reviews of adapogenic and medicinal plants with potential effect on spinal cord injuries ( Zhang2016tet ) and Parkinsonism ( Fu2015pna ) highlight resveratrol, curcumin , tea polyphenols, ligustrazine from Lingusticum chuanxiong , flavonoid quercetin present in vegetables and fruit, Pueraria lobata ) and ginseng.
  • The list of plants potentially effective against Alzheimer's disease ( Hugel2015bfa ) mentions turmeric, Salvia miltiorrhiza , ginseng, cinnamon, coriander, rosemary, sage and other deworms commonly used as spices.
  • Glossy glamor protects memory and its associated hippocampal neurons ( Zhou2012nep , Aguirremoreno2011glr ). It also protects dopaminergic neurons ( Ding2010gle ), whose death is caused by Parkinsonism . Since these neurons are among the most sensitive, it can be expected that glossy shield protects neurons in general, see, for example, Zhang2011tna .
  • Pink rosette counted against autoimmune brain damage ( Zhu2016saa ).
  • Baikal Shihak has pronounced neuroprotective effects demonstrated in cerebral ischemia and stroke models ( Gaire2014sbs ). Its active ingredient bajcalin protects against cognitive impairment in diabetes ( Ma2015bad ) and its protective effect on the neurons of the hippocampal memory center ( Lim2016asb ) has been identified.
  • Chinese Koptis ( Zhang2009btb ) and other plants TČM.

The plant with these effects must, of course, be much more than I can mention and document in this short paragraph. In addition, there are new reports every year on this topic, so I have to refer you to the primary sources for the latest information. Note, however, that many neuroprotective substances come from spices (curcumin and others) or common foods (resveratrol, quercetin). I would therefore like to draw attention to the book "Spices and Its Medicinal Effects" by the famous prof. Pavel Valíček, where the healing effects of spices are documented more systematically.

| 4.11.2018