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Neuroprotection 3 –

bebeto1
24.09.2018

Content:

  • Neuroprotection 3 –
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  • Neuroprotection in Glaucoma: Old and New Promising Treatments
  • Some other stimulants, in appropriate doses, can however be neuroprotective. Selegiline: It has been shown to slow early progression of. We review the mechanisms by which hypothermia confers neuroprotection as .. Therapeutic hypothermia consists of 3 phases: induction, maintenance, and. Neuroprotective and disease-modifying effects of the ketogenic diet . A third variation on the diet, known as the Radcliffe Infirmary diet, represents a.

    Neuroprotection 3 –

    This review illustrates some of these old and new promising agents for the adjuvant treatment of POAG, with particular emphasis on forskolin and melatonin. Glaucoma is a worldwide leading cause of irreversible blindness.

    It is a multifactorial optic neuropathy characterized by the progressive loss of retinal ganglion cells RGCs and their axons [ 1 ]. Although the etiopathogenesis of glaucoma is not fully understood, high intraocular pressure IOP appears to be related to RGC death, both in the case of acute closed-angle glaucoma, when there is a sudden increase of IOP, and in the case of primary open-angle glaucoma POAG , which develops relatively slowly over the years.

    In glaucomatous patients, the increased resistance to aqueous drainage through the trabecular meshwork POAG and the obstruction of the drainage pathway by the iris primary closed-angle glaucoma are the main causes of IOP elevation [ 4 , 5 ].

    Furthermore, several risk factors have been associated with glaucoma pathogenesis: The growing knowledge of this disease and its etiopathogenesis has prompted the study of new targets and therapeutic agents aimed at stopping or delaying RGC neurodegeneration Figure 1 b. The goal of the present review is to discuss some of the old and promising new agents that may contribute to a better treatment of POAG.

    The major risk factors linked to the starting of the chain of events finally leading to overt POAG may be of genetic, mechanical, biochemical, or hemorheological nature.

    None of them by itself can explain or predict the insurgence and progression of the disease, which is most likely controlled by a combination of different factors, some of which probably still need to be identified.

    A certain degree of familiarity exists for POAG, which has led to the discovery of several genes that may be associated with the disease [ 9 ]; however, no single gene by itself has been found to cause POAG. IOP increase is the main mechanical risk factor, which may stress both retinal layers and the lamina cribrosa through which RGC nerve fibers leave the eye, forming the optic nerve.

    This may result in ischemic injury, glial cell activation, reduced axoplasm flow, and neurotrophin deprivation, finally causing RGC apoptosis [ 10 ]. Further glutamate release from dying cells may cause an excitotoxic response in neighboring RGCs, triggering their apoptotic death in a vicious circle [ 11 ].

    Oxidative stress induced by oxygen and nitrogen reactive species is also implicated in the etiology of POAG and several other eye disorders [ 12 — 15 ]. Several mechanisms involving antioxidant enzymes such as superoxide dismutase SOD , as well as antioxidants such as glutathione and ascorbate, protect the eye from oxidative stress [ 16 ].

    It has been found that POAG patients exhibit low levels of circulating glutathione, suggesting a general impairment of the antioxidative defense [ 17 ], while reduced expression of the antioxidant enzymes SOD and glutathione S-transferases was found in the aqueous humor of POAG patients, suggesting that this state could aggravate the balance between both oxygen- and nitrogen-derived free radical production and their detoxification.

    Defective blood perfusion of the retina and the optic nerve head may also be critical factors in POAG development and progression, with more relevance in the case of NTG [ 18 ]. Despite the identification of several risk factors for POAG, the main—if not the only—therapeutic target to treat glaucoma still remains the IOP.

    Even though clinical studies have shown that decreasing the IOP is necessary, it is not the only condition capable of preventing glaucoma development or progression [ 4 ]. Therefore, neuroprotection strategies have been developed in recent years, not to replace but to complement the classical IOP lowering approach [ 19 ], aiming at slowing down POAG progression.

    Several targets have been proposed for neuroprotection, and molecules acting on such targets can be classified as oligopotent or multipotent, depending on whether they may act on multiple targets or not. We have chosen here a selection of molecules belonging to either class, mostly based on our direct experience with them Figure 2.

    Forskolin is a diterpene isolated from the root extract of Coleus forskohlii species [ 20 ]. It is a receptor-independent activator of adenylate cyclase.

    In forskolin-treated cells, the intracellular concentration of the second messenger cAMP is rapidly increased [ 21 ]. The adenylate cyclase complex is present both in ciliary body epithelial cells [ 22 ], deputed at producing the aqueous humor AH , and in trabecular meshwork TM cells, regulating the aqueous humor outflow [ 23 ]. Numerous studies have shown that forskolin is able to reduce IOP in animals and humans [ 24 — 32 ]. This happens probably because cAMP elevation in the ciliary body may lead to the activation of the chloride maxi channel in pigmented epithelial cells, facing the stroma, thus leading to resorption of AH from the posterior chamber into the stroma Figure 3 a [ 33 ].

    Conversely, alpha-agonists and beta-blockers decrease cAMP production in nonpigmented epithelial cells, thus decreasing the activity of the chloride channels facing the posterior chamber, leading to decreased AH secretion Figure 3 a [ 34 ]. Therefore, forskolin treatment results in a reduced amount of AH accumulation in the anterior chamber decreased secretion and increased outflow in response to adenyl cyclase activation [ 27 , 37 ].

    Interestingly, the reduction of IOP by forskolin occurs through mechanisms that are not fully exploited by the existing hypotonizing glaucoma drugs.

    In fact, glaucoma patients, in whom the target pressure could not be reached even by the combination of three or four hypotonizing drugs, experienced a further decrease of their IOP when oral forskolin was added to their therapy [ 38 ]. Beyond its action on IOP, forskolin may exert direct neuroprotection through different mechanisms. In a rat model of experimental glaucoma, artificial elevation of IOP cripples the optic nerve head at the level of the lamina cribrosa, swelling nerve fibers and blocking the axonal flow of BDNF, while expression of the cognate receptor TrkB is increased at the optic nerve head [ 42 ].

    Similar findings have also been reported in a spontaneous glaucoma model in the American Cocker Spaniel dog [ 43 ]. In this respect, forskolin could provide some degree of direct neuroprotection through the activation of paracrine signaling, since it has been shown to induce BDNF expression by astrocytes and vascular endothelial cells [ 44 , 45 ] and to promote translocation of the cognate receptor TrkB to the neuron cell membrane [ 46 ].

    Moreover, forskolin has been shown to be necessary for neuron cell survival in vitro [ 47 , 48 ]. Also, optic nerve regeneration that is promoted by oncomodulin needs cAMP elevation as it can be promoted by forskolin in order to work efficiently [ 49 — 51 ]. Finally, elevation of cAMP levels is known to reduce excitotoxic damage and to inhibit the resulting apoptotic cell death [ 52 ]. Forskolin has been shown to protect neuronal cell cultures from soman and sarin, which are toxic organophosphate chemicals [ 53 ], and to attenuate the adverse effects of long-term Schwann cell denervation on peripheral nerve regeneration in vivo [ 54 ].

    Homotaurine has been reported to decrease the accumulation of amyloid plaques in neurons [ 59 ], and carnosine has shown extensive neuroprotective efficacy in a rat model of experimental glaucoma [ 60 ]. Therefore, based on these results, the synergic neuroprotective effect of forskolin, homotaurine, and L-carnosine has been investigated in a rat model of experimental glaucoma [ 61 ]. Such neuroprotective effect is also correlated with the reduction of calpain activity, known to be linked to neurodegenerative events [ 66 , 67 ].

    Support of the above comes from a recent clinical study [ 68 ] carried out on glaucomatous patients with IOP compensated by topical drugs, which evaluated the additional neuroprotective effect of the food supplement containing forskolin, homotaurine, carnosine, folic acid, vitamins B1, B2, and B6, and magnesium.

    Treatment with the food supplement resulted in a further significant decrease of the IOP most likely due to forskolin and an improvement of PERG amplitude and foveal sensitivity, parameters related to RGC function. Saffron is derived from the pistils of Crocus sativus , a well-known traditional Chinese medicine [ 69 ], and contains high concentrations of the carotenoids crocin and crocetin. Multiple divalent carbon bonds in saffron compounds confer their powerful radical scavenging and antioxidative properties [ 70 — 72 ].

    It is likely because of this antioxidant effect on a clogged trabecular meshwork that high dose oral saffron treatment may further decrease IOP in POAG patients already undergoing different hypotonizing treatments [ 73 ]. More recent studies have highlighted the neuroprotective properties of saffron. In a rat model of continuous blue light exposure, saffron dietary supplement protects photoreceptors from photooxidative damage, maintaining both morphology and function [ 74 ].

    Similar results against light-induced damage were obtained in mice and were attributed to the inhibition of caspase activity [ 75 ]. The main saffron components of interest for their associated biological activity are the carotenoid derivatives crocetin and crocin [ 69 ]. Ocular hypertension, as well as the consequent reduced blood flow into the eye circulation, is the basis for the longstanding ischemic hypothesis of glaucoma [ 77 , 78 ]. Crocin improves both the retinal and the choroidal blood flow in vivo and consequently facilitates retinal function recovery following IOP increase [ 79 ].

    Experimental studies have shown that brimonidine has also neuroprotective activity. In a retinal ischemia model, the intraperitoneal administration of brimonidine prevented the accumulation of toxic concentrations of extracellular glutamate and aspartate and preserved the ERG-b wave [ 86 ]. Similarly, systemic treatment with brimonidine prevented the elevation of N-methyl-D-aspartate NMDA receptor expression in rat ischemic retinal injury induced by acute IOP elevation [ 87 ] and limited RGC death in both an isolated rat retina and an in vivo rabbit retinal excitotoxicity model, through the modulation of the NMDA receptor function [ 88 ].

    Systemic administration of brimonidine has been shown to protect RGC in a rat model in which chronic ocular hypertension was induced by laser photocoagulation of the trabeculae [ 89 ]. Brimonidine has been shown to upregulate neurotrophic factors expression in the retina, such as fibroblast growth factor 2 FGF2 and BDNF [ 90 , 91 ]. The neuroprotective effects of brimonidine on RGC are also evident after topic ocular administration in adult rats [ 92 ]. Clinical studies have shown that topical brimonidine improved the visual outcome of patients undergoing laser treatment for classic extrafoveal or juxtafoveal choroidal neovascularization treatment [ 93 ] and that brimonidine, but not timolol, topical therapy, improved contrast sensitivity of glaucoma patients after 3 months of treatment [ 94 ].

    More recently, a long-term clinical study has indicated that topical brimonidine treatment may indeed protect the RGC of glaucomatous patients. The clinical comparison between brimonidine and timolol in preserving the visual function of NTG patients over a period of 4 years of observation has shown that, despite an identical effect on IOP, after 2 years, those patients treated with brimonidine were less likely to have disease progression than those treated with timolol [ 95 ].

    Citicoline is a naturally occurring cell endogenous compound, intermediate in the synthesis of membrane phospholipids such as phosphatidylcholine [ 96 ]. Experimental studies have shown that citicoline may indeed increase the synthesis of phospholipids in the CNS [ 97 ] and indicated a neuromodulator effect and a protective role of this molecule on RGC [ 98 ]. In rodent retinal cultures and animal models, citicoline triggered antiapoptotic effects, increased the retinal level of dopamine one of the most important neurotransmitters involved in retinal and postretinal visual pathways [ 99 ], and prevented the thinning of retinal nerve fiber layer [ ].

    However, whether dopamine itself works as a neuroprotectant for RGC is not clear yet, since no direct effects of dopamine on RGC survival have been reported. Citicoline has been shown to protect the retina in vivo against kainate-induced neurotoxicity [ ] and to rescue rat RGC following partial optic nerve crush [ ].

    A beneficial effect of citicoline oral supplement has been demonstrated in patients with nonarteritic ischemic optic neuropathy. At the end of the study, PERG, visual evoked potentials, and visual acuity were improved compared to pretreatment values and to a group of patients with no treatment during the same period [ ].

    Other clinical studies reported citicoline neurotrophic effects in POAG management [ — ]. Ongoing laboratory measurements include blood gases, liver function tests, CPK, and electrolytes, as well as close monitoring of input and output. Good cardiac output and blood pressure are maintained to optimize brain perfusion. Acidosis and electrolyte imbalances are corrected, and normal glucose levels are preserved.

    Many of these infants require ventilator support as well as pressor support in order to achieve good oxygenation and perfusion. Several of our infants have required advanced respiratory support, including inhaled nitric oxide and extracorporeal membrane oxygenation ECMO for support of their pulmonary and cardiovascular systems. Nursing care for hypothermia therapy includes close monitoring of neurologic status, and observation for clinical or sub-clinical seizures on aEEG.

    The nursing staff observes the infants for pain as well as any complications due to skin exposure to the cap or blanket. Close monitoring of vital signs, and assessment of respiratory and cardiac stability is key the care of these infants.

    After 72 hours, the infant is warmed slowly. Careful attention is given to the aEEG at this time, because seizures may occur during rewarming. After the course of hypothermia, an MRI is obtained for structural assessment and a traditional EEG is used to examine function. During the recovery period occupational therapy and physical therapy are closely involved with families to help infants with residual feeding and tone problems.

    Once children are discharged, they are followed closely in neurodevelopmental follow up clinic. Our infants are followed for a minimum of 18 months, and preferably for three to four years.

    Many of these children are just approaching school age, and school performance will be a critical metric of this technique. There is growing evidence that hypothermia can be used in the perinatal period to reduce cerebral injury and improve neurological outcome in infants who have HIE. Although the major clinical trials were performed well, unanswered questions remain. In addition, a significant proportion of infants may have had chronic injury that began in utero plus additional acute injury at birth.

    These unknowns, as well as the extent of the initial injury, may contribute significantly to the variability in outcome following treatment.

    This article is Open Access. Please wait while we load your content Back to tab navigation Download options Please wait Supplementary information PDF K. Synthesis and biological evaluation of 2,2-dimethylbenzopyran derivatives as potent neuroprotection agents F. For reproduction of material from NJC: For reproduction of material from PCCP: For reproduction of material from PPS: For reproduction of material from all other RSC journals:

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    Caspase 3 activation is essential for neuroprotection in preconditioning. BethAnn McLaughlin, Karen A. Hartnett, Joseph A. Erhardt, Jeffrey J. Legos, Ray F. Dickkopf-3 (Dkk3) is an atypical member of the Dkk family of Wnt inhibitors, which has been implicated in the pathophysiology of neurodegenerative disorders. be reached within about 4 weeks. 8 Typically the increase in. Neuroprotection for the Warrior: Dietary Supplementation. With Omega-3 Fatty Acids. COL Michael.

    Neuroprotection in Glaucoma: Old and New Promising Treatments



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    Caspase 3 activation is essential for neuroprotection in preconditioning. BethAnn McLaughlin, Karen A. Hartnett, Joseph A. Erhardt, Jeffrey J. Legos, Ray F.

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