Why Supplement with ENZYMES. Enzyme supplements are not destroyed by stomach acid. Anyone who eats cooked or processed food requires. The 'Miracle' Enzyme™ is Serrapeptase, the 2nd Gift from Silkworms Giving and appropriate enzyme activity, there can be no return to health. This is. The 'Miracle' Enzyme™ is Serrapeptase, the 2nd Gift from Silkworms Giving the succeed with the inclusion of enzymes and nutrition as part of those plans?”.
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MIRACLE ENZYMES SERRAPEPTASE AND NATTOKINASE MITIGATE NEUROINFLAMMATION AND APOPTOSIS ASSOCIATED WITH ALZHEIMER'S. Download PDF The Enzyme Factor | PDF books Ebook Free Download the idea of a miracle enzyme out of which all the enzymes the body. Editorial Reviews. From Publishers Weekly. A bestseller in Shinya's native Japan , where it was In Your Bodys Miracle Enzyme, Dr. Hiromi Shinya presents hisresearch, grounded in his 45 years of medical practice in the UnitedStates and .
Regarding the groups treated with either serrapeptase or nattokinase in different doses, our findings showed significant www. These results are greatly supported by the histological findings. Thus, it could be concluded that serrapeptase and nattokinase may be considered as newly neuroprotective agents against inflammation and apoptosis characterizing AD through their proteolytic, anti-inflammatory and anti-apoptotic effects.
Key Words: This disease accounts for 50 to 80 percent of dementia cases. Symptoms of AD usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. Neither AD etiology nor the onset of AD pathology is totally understood.
Additional risk factors such as increasing cholesterol and homocysteine levels as well as chronic exposure to several minor metal ions such as aluminium, copper and iron are also linked to AD Bharathi et al.
Apart from the pathological hallmarks of the disease, AD brain exhibits constant evidence of ROS mediated injury Buizza et al. In addition, cerebral inflammation and systemic immunological alterations have a role in AD pathogenesis Salminen et al. The inflammatory changes include activation of microglia and astrocytes and infiltrating inflammatory cells with increased levels of proinflammatory cytokines Galasko and Montine, and Fadel et al. World Journal of Pharmacy and Pharmaceutical Sciences and their caregivers.
Today, there is a worldwide effort under way to find better ways to treat the disease, delay its onset and prevent it from developing.
Proteolytic enzymes work to aid the body in digesting proteins. Proteolytic enzymes are produced naturally in the pancreas but may also be found in certain foods.
Supplements containing these enzymes may be used to address a variety of health concerns Fadel et al. Serrapeptase is a 50 kDa metallprotease that has gained wide acceptance in Asia and Europe as a potent analgesic and anti-inflammatory drug. Serrapeptase is being used to treat chronic inflammatory disease such as atherosclerosis, arthritis, bronchitis, fibrocystic breast disease and sinusitis Klein and Kullich, Serrapeptase is an immunologically active enzyme and it can bind itself to the alpha 2 macroglobulin in our plasma where it is shielded from the immune system while retaining its enzymatic activity, and in this way it is transferred to the sites where it is needed in the body Mazzone et al.
The thrombolytic activity of nattokinase has been found to be stronger than that of plasmin or elastase both in vitro and in vivo Chang et al.
In some aspects, NK is actually superior to conventional clot-dissolving drugs, as it has many benefits such as convenient oral administration, more efficient, prolonged effects and prevention of clot formation. Nattokinase has been demonstrated to have pH and temperature stability and so can be found in the gastrointestinal tract Zheng, et al. The selected doses of the two proteolytic enzymes used in the present study were equivalent to the human recommended doses and converted to rat equivalent with the help of Paget equation Paget and Barnes, Aluminum chloride AlCl3 was downloadd from Sigma Co.
The molecular weight of AlCl3 is The animals were subjected to standard diet and water ad libitum. All animals were accommodated with laboratory conditions for at least two weeks before the experiment and maintained under the same conditions all over the experimental period.
All animals received human care and use according to the guidelines for Animal Experiments which were approved by the Institutional Animal Ethics Committee, National Research Centre, Egypt. Experimental Design Sixty male albino rats weighing g were randomly classified into six groups, with ten animals in each group; Group 1: At the end of the experimental period, the animals were fasted overnight, sacrificed by decapitation under diethyl ether anesthesia.
The whole brain of each rat was rapidly and www. World Journal of Pharmacy and Pharmaceutical Sciences carefully dissected, thoroughly washed with isotonic saline and dried on filter paper.
The homogenate was centrifuged at xg for 10 min. Quantitative estimation of total protein content in the brain was carried out according to the method of Lowry et al. Washing was done in tap water, then serial dilutions of alcohol methyl, ethyl and absolute ethyl were used for dehydration. The specimens were cleared in xylene and embedded in paraffin at 56 degree in hot air oven for twenty four hours.
Paraffin bees wax tissue blocks were prepared for sectioning at 4 microns by slidge microtome. The obtained tissue sections were collected on glass slides ,deparaffinized and stained with hematoxylin and eosin stains Banchroft et al. Then, the slides were examined under the light microscope. World Journal of Pharmacy and Pharmaceutical Sciences program, version 11 followed by least significant difference to compare the significance between groups Armitage and Berry, In contrast, the groups of rats that administered with low or high dose of serrapeptase The protective effect of serrapeptase and nattokinase on brain cholinesterase activity in rat model of Alzheimer's disease.
Table 2: The protective effect of serrapeptase and nattokinase on brain Bcl-2 and P53 levels in rat model of Alzheimer's diseases.
Fig 2: Microscopic examination of brain tissue sections of control rats showing the normal histological structure of the cerebellum cr. Fig 5 Fig 6 Fig 7 Fig 8 Fig 5 Microscopic examination of brain tissue sections of rat model of AD protected with low dose of serrapaptase showing focal gliosis in cerebral cortex g. Fig 6 Microscopic examination of brain tissue sections of rat model of AD protected with low dose of serrapaptase showing focal gliosis g and congestion in cerebral blood capillaries of the cerebrum.
Microscopic examination of brain tissue sections of rat model of AD protected with high dose of serrapaptase showing plaque formation P in the striatum. Microscopic examination of brain tissue sections of rat model of AD protected with high dose of nattokinase showing focal gliosis in cebral cortex g.
Microscopic examination of brain tissue sections of rat model of AD protected with high dose of nattokinase showing capillary congestion with perivascular oedema in the striatum.
Acetylcholine is a neurotransmitter a brain chemical that helps with memory and thinking. Alzheimer's disease breaks down acetylcholine.
And people who have Alzheimer's disease make less of this chemical over time. These two things result in the gradual loss of memory and thinking skills Tabet et al. The present study revealed that, AlCl3 administration shows significant elevation in brain cholinesterase AChE activity.
Acetylcholiesterase AChE itself has been implicated in the pathogenesis of Alzheimer's disease. In particular, it appears that AChE may directly interact with amyloid-beta in manner that increases the deposition of this peptide into insoluble plaques. This finding is in agreement with that of Zhang et al. Hydrogen peroxide acts as a modulator in the activity of functionally important proteins, receptors and enzymes Kamster and Segal, There is increasing evidence that neurotoxicity in AD is mediated by inflammatory processes McGeer et al.
World Journal of Pharmacy and Pharmaceutical Sciences for the amyloid precursor protein. The present results revealed a significant elevation in brain IL-6 in AlCl3 administered group which is in agreement with Weaver et al. IL-6 was found not only in plaques, but also around the bodies of isocortical neurons, only in AD. A growing body of evidence suggested that the dysregulation of IL-6 contributes to the development of AD Combarros et al.
Furthermore, Cojocaru et al. There is a growing body of evidence which supports the hypothesis of immune regulation and autoimmunity or inflammatory processes as vital mechanisms in the pathogenesis of the disease.
DNA- end labeling technique suggests that some neurons die by apoptosis. Numerous apoptosis regulating factors have been identified; these are represented in Bcl-2 family, apoptotic protease activating factors, caspase family, P53 and nuclear factor- kB Kitamura et al. The present results showed a significant decrease in brain Bcl-2 and an increase in brain P levels in AlCl3 administered group as compared to the control one.
Bharathi et al. All these events lead to genomic instability and cell death. Our results could be explained as P53 has a critical regulatory function at the G1-cell cycle www. It has been reported that P53 protein induces the upregulation of pro-apoptotic Bax and the downregulation of anti-apoptotic Bcl-2 in the hippocampal neurons Kitamura et al.
In the view of the obtained results, the significant inhibition of brain AchE activity due to co- treatment with serrapeptase or nattokinase during AlCl3 supplementation for 45 days, could be explained by the antiamyloidogenic effect of these two enzymes Fadl et al. Moreover, serrapeptase and nattokinase have been reported to have antioxidant potential Fadl et al. By these ways, both serrapeptase and nattokinase could ameliorate AChE activity in the brain.
Co-treatment with serrapeptase or nattokinase plus AlCl3 for 45days in the present study resulted in significant increase Bcl-2 associated with significant decrease in P53 in the brain tissue. This property www. World Journal of Pharmacy and Pharmaceutical Sciences leads to amelioration of neuronal death and restoration of brain Bcl-2 level. Additionally, the antioxidant activity of both serrapeptase and nattokinase Davies, plays an important role in correcting brain levels of Bcl-2 and P As these enzymes have the ability to prevent ROS accumulation in the brain through their free radical scavenging effects, which have a major contribution in the neuronal death.
Thus, serrapeptase and nattokinase could modulate neuronal apotosis via restoration of the mitochondrial membrane permeability and in turn mitochondrial function that finally lead to the preservation of Bcl-2 and suppression of P53 brain levels. The biochemical findings in the present study were well documented by our histological results which showed the formation of cerebral encephalomelacia with plaques formation, neuronal degeneration and oedema with gliosis in AlCl3 administered group.
This indicted that this is a good model for AD-like pathology. These findings are merging with the previous studies Kawahara et al. Regarding the peotective effect of serrapeptase and nattokinase, it is clear from the pathological investigation the disappearance of most of the amyloid plaques.
In conclusion, the present study provides a strong evidence that serrapeptase and nattokinase have potent protective effect against AD in AD like pathology model. Armitage P. Comparison of several groups. Statistical method in medical research. Oxford, UK: Blackwell Science Ltd, ; pp.
Banchroft J. And Turner D. Theory and Practice of Histoloicl Techniques.
World Journal of Pharmacy and Pharmaceutical Sciences 3. Barbareschi M. Bcl-2 and P53 expression in node negative breast carcinoma a study with long term follow up. Human Pathol. Barron J.
Natural health news and community, Bauer J and Herrmann F. Interleukin-6 in clinical medicine. Hematology, Bharathi, P. Vasudevaraju, M. Govindaraju, A. Palanisamy, K. RNA prep- arations from untreated T cells from two healthy blood bank donors and from the same T cell population treated with antibodies against CD3 and CD28 for 72 h were subjected to Northern blotting using FX-specific probes.
Expression of fucosyl transferase VII by resting and activation also caused a significant increase in FX ex- activated T cells.
The pression P , 0. These results were con- Since Th1 and Th2 cells differ in their expression firmed in this study Fig. It was of interest, there- profiles for fucosyltransferases and for selectin ligands fore, to examine whether, similarly to T cells, B cells 14, 19, 20 , we assayed the expression levels of FX in also would express up-regulated levels of FX upon ac- antigen-driven activated Th1 and Th2 cells and found tivation.
This indicates that the differ- ence in selectin ligand expression between Th1 and Th2 cells 14, 19, 20 cannot be ascribed to differences in FX expression. Expression of sLe-a and sLe-x by resting and activated B Methods.
RNA from these cells was subjected to Northern blotting. B cell activation significantly up-regulated the two cell types.
B cells were treated with anti-IgM leads to a twofold reduction of the FX protein com- antibodies for 72 h. RNA from these cells or from untreated resting pared to control oligonucleotides Fig. To evalu- cells was then subjected to Northern blotting. The treatment signif- ate whether a cause and effect relationship exists icantly increased FX mRNA expression in the activated cells.
This treatment caused a sig- jected to a B cell enrichment procedure using anti- nificant fourfold, P , 0. This experiment was performed twice using B tions depends upon specific patterns of adhesion mol- cells from two different donors.
Similar results were ecule expression by these lymphocytes The bind- obtained in both experiments. FX antisense as oligonucleotide mediated down-regulation of FX and of selectin ligand expression in activated T cells. The reduction in the expression of these selectin ligands was evaluated by arbitrarily multiplying the value of mean fluorescence flu. It should be noted that both flow cytometry parameters were reduced in FX antisense-treated cells.
Diverse cell types such as Th1, Th2, or regulate selectin ligand expression in activated T cells B, as well as HNSCC 12 , although activated through 14, 18 —20, 24, For example, a single fucosyltrans- different receptors, all express up-regulated levels of ferase, FucT-VII, was shown to control the synthesis of this enzyme regardless of the receptor delivering the E-selectin ligands on activated T cells Rolling of activation signal.
The rolling was mediated by selectin cell—matrix interactions 29 — The up-regulation of ligands expressed by the transfectants In con- the fucose-generating FX enzyme in various cells by trast, the expression of carbohydrate determinants in- outside-in signaling may thus influence the expression volved in the binding of B cells to E- and P-selectins, levels of such glyconjugates and the interactions medi- does not correlate with the induction of any of the ated by these molecules.
The active role played by FX in the regulation of The results of the present study demonstrate that an selectin ligand expression, and possibly also that of additional factor, the FX enzyme, takes part in the additional glycoconjugates, makes it a potential novel regulation cascade of selectin ligand expression by ac- target for modulation of inflammatory processes, auto- tivated lymphocytes.
We showed that polyclonal acti- immune diseases, and possibly certain types of cancer. Eshel is a Marnie Kimelman fellow. Witz is the incumbent of the David Furman Chair in Immuno- ery of outside—in activation signals to lymphocytes up- biology of Cancer.
Vestweber, D. Cell Biol. Lasky, L. Johnson-Leger, C. Ebnet, K.
This suggests that FX is an up- trol leukocyte extravasation: The selectins and the chemokines. Brandley, B. Cell 63, — , Springer, T. Several studies have indicated that the mechanism Nature , —, Walz, G. In both cases the binding of the extravasating cells eloid and tumor cells. Science , —, Sullivan, F.
In support of such a mecha- J. A causative link was found Chem.
++Serrapeptase The Miracle Enzyme
Ohyama, C. Stimulatory sig- J. Marquardt, T. Van Wely, C.
Blood 94, —, Bio- Brinkman-Van der Linden, E. Sambrook, J. Eshel, R. Lefkovits, I. Witz, I. Today 21, —, Brakenhoff, R.The two most common treatments for inflammation are steroids such as Prednisone and non-steroidal anti-inflammatory drugs, called NSAIDs, such as over-the-counter aspirin, ibuprofen Advil, Motrin , ketoprofen Orudis , naproxen sodium Aleve , and over eleven prescription NSAIDs.
Also consider trying high potency forms , units for best results and start with a low daily dose, working upwards within reason too many a day can tax your liver , until you see results for your condition.
miracle enzyme.pdf - Serratiopeptidase The Miracle Enzyme...
E and Griffinb S. The protective effect of serrapeptase and nattokinase on brain cholinesterase activity in rat model of Alzheimer's disease. Interleukin-6 and risk of cognitive decline. Neri, B. Clipping is a handy way to collect important slides you want to go back to later. P, and Singhal R.
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