Research Progress On Neuroprotective Effects Of Hyperbaric Oxygen And Cistanche

Abstract

Hyperbaric oxygen therapy, which involves intermittently breathing 100% oxygen at pressures above sea level, has been shown to have some neuroprotective effects and is used to treat a wide range of neurological disorders. This paper reviews the neuroprotective effects and molecular mechanisms of hyperbaric oxygen therapy in different neurological disease models. To explore the effect of cistanche on the oxygen supply capacity of the brain.

Key words

Cistanche; apoptosis; clinical trial; hyperbaric oxygen; inflammation; in vitro; in vivo; neuroprotection; oxidative stress

Introduction

Limited by effective treatment strategies, neurological diseases are one of the leading causes of death and disability worldwide. Although promising strategies have been reported in animal models of neurological diseases, they often fail to work in clinical practice. Therefore, new treatment strategies need to be developed and developed. Over the past few decades, various drug compounds as well as various treatments with neuroprotective effects have been described, including hyperbaric oxygen therapy as a non-drug and non-invasive treatment. Hyperbaric oxygen (HBO) therapy (HBOT) is defined as intermittent breathing of pure oxygen in a high-pressure chamber above sea level. During HBOT, the amount of dissolved oxygen in the plasma, as well as the amount of oxygen-saturated hemoglobin, increases, causing the organs to receive more oxygen. HBOT has been shown to have neuroprotective effects on experimental spinal cord injury (SCI), 3 brain injuries, 4 to 5 neurodegenerative diseases, 6 to 7 peripheral nerve injuries, 8 to 9, and neurotoxic models On the other hand, the clinical evidence supporting the neuroprotective properties of HBOT is limited. In addition to improving oxygen supply and neurometabolism, the beneficial effects on various biological characteristics are mainly the correlation between antioxidant, anti-inflammatory and anti-apoptotic properties. At the same time, cistanche has the role of vasodilating, and whether it can increase the ability of hemoglobin support for the treatment of neurological diseases is worth studying.

Pic: Faw Cistanche

Brain injury

Studies have shown that brain injury after stroke or trauma is due to a variety of pathophysiological processes such as nitrification and oxidative stress, disruption of the blood-brain barrier (BBB), excitatory toxicity, nerve cell death, inflammatory responses, and angiogenesis defects. 51-53 In this regard, Weinstein et al.54 showed that HBOT had a significant protective effect against death from untreated cerebral ischemia in anesthetized gerbils, while histological examination showed that the degree of patchlike bilateral ischemic neuron damage was much less in surviving gerbils receiving HBOT. Subsequently, a study was conducted to determine the effects of HBOT on free radical generation and lipid peroxidation after global cerebral ischemia. The results of this study showed that HBOT can increase oxygen free radical levels after cerebral ischemia, but not accompanied by increased lipid peroxidation and decreased neurophysiological recovery. In fact, despite the initial increase in free radical production, the amount of peroxidation was similar to that in the control group, and the coverage of dermoplast sensory evoked potential recovery in the HBOT treated animals was more than 50 times greater than in the control group.

Another study showed that hyperbaric oxygen reduced blood flow and cerebrovascular permeability after global cerebral ischemia in rabbits, but the recovery of somatosensory evoked potential was the same as in the control and hyperbaric oxygen groups. However, in another study, HBOT had no beneficial effect on neurological outcomes after acute focal cerebral ischemia. Adult rats with middle cerebral artery occlusion showed improvement in motor injury after immediate or delayed 60-minute exposure to hyperbaric oxygen, as well as a reduction in cerebral infarction. Evaluation of the effect of neutrophils and prophylactic HBO on brain injury showed an absolute preischemic HBOT concentration of 2.8 atmos (ATA; 1 ATA = 101.325 kPa) after 45 min, by inhibiting neutrophil isolation, the concentration of myeloperoxidase, functional neurological impairment, and cerebral infarction volume were reduced. HBOT can regulate the changes of excitatory amino acids and brain energy metabolites during cerebral ischemia at different time after ischemia. Neurotrophin-3 has a protective effect on neuronal cell death during cerebral ischemia response. In this regard, it has been shown that HBOT reduces the regulation of postischemic neurotrophin-3 mRNA in rat hippocampus. HBOT has a dual effect on cerebral infarction, and it may be beneficial to use HBOT within 6 hours after ischemia-reperfusion injury, but harmful to use HBOT after 12 hours or longer after injury. However, HBOT did not reduce tissue damage within 4 hours of permanent focal cerebral ischemia. Yin et al. 63 found that HBOT could inhibit the overexpression of cyclooxygenase-2 in cerebral cortex after cerebral ischemia. HBOT improved exercise scores and reduced brain edema after TBI, as well as decreased inflammatorome components of IL 1β, IL 18, and NLRP 3. The results showed that HBO de increased inflammation by modulating NLRP-3 - inflammasome signaling in microglia. After middle cerebral artery occlusion in hyperglycemic rats, HBOT reduces hemorrhagic transformation and infarct volume via ATP/NAD+ /Sirt1 pathway, which may be a promising approach for patients with diabetic acute ischemic stroke. Multiple HBOT sig significantly reduces the expression of c-jun, c-fos and Bax. And increased the expression of Bcl-2, neurotrophin 3, neurotrophin derived from glial cell lines, BDNF, and nerve growth factor 111 In addition, The blood-brain barrier permeability of rats after global cerebral ischemia/reperfusion injury was improved by increasing HBO exposure of tight junction proteins zonula Occlgens-1 and caveolin-1. 112He et al.113 found that HBOT attenuated neu ronal apoptosis after traumatic brain injury through the Akt/GSK3β/β-catenin pathway.

A final set of experiments showed that hemoglobin levels of oxygen were higher in mice fed cistanche extract than in mice not given the extract. This indicates that cistanche has the effect of increasing hemoglobin oxygen content.

Pic: Effects of Cistanche treat Alzheimer‘s disease

Nerve injury

Muscle paralysis and neuropathic pain due to destruction of motor and sensory neurons are the most common symptoms of nerve injury. Meanwhile, neuroinflammation, oxidative stress, excitatory toxicity, apoptosis and loss of neurotrophic support are some of the mechanisms of neurodegeneration after nerve injury. In this regard, a rat model of sciatic nerve was used to evaluate the effect of HBOT on healing after peripheral nerve damage. The results of this study showed that HBOT promoted functional recovery of transverse peripheral nerve after 1 week of microsurgical repair. In addition, another study concluded that HBOT effectively prevents fiber ischemia despite rats with peroneal nerve compression and transverse injury without HBOT associated changes in nerve/muscle force measurements and edema. However, a study on the effect of hyperbaric oxygen on the regeneration of crushed sciatic nerve injury showed that 100% oxygenated therapy under pressure promoted peripheral nerve healing in rabbits. HBOT(first at 0, 4, and 8 h postoperatively, then every 8 h) stimulated axonal out growth after sciatic nerve compression injury in rats. The needling reflex test and nerve filament staining were used for assessment. However, another study using walk path analysis showed that HBOT(twice daily for 3 days) had no effect on functional recovery after crush injury to the standard sciatic nerve in rats. Subsequently, several researchers studied the effects of HBOT on the axon growth of rat sciatic nerve cells and non-cellular nerve grafts. Axonal growth was significantly prolonged in animals treated with HBOT after cellular nerve transplantation, compared with acellular nerve transplantation, which had no beneficial effect on axonal growth.

Another study confirmed that HBOT did not restore gait or muscle strength 90 days after nerve transection and repair or nerve crush injury in rats. It was found that HBOT could inhibit the changes of Na+ and K+ -ATPase activities in the optic nerve of ischemic rats after HBOT administration, but the SOD activity level in the optic nerve of ischemic rats did not change. Long-term effects of hyperbaric oxygen on transected sciatic nerve and microsurgical repair were evaluated. Function recovered after 7 weeks.

The last set of studies showed that echinacoside has a concentration-dependent relaxation effect on the thoracic aortic vascular ring pretreated with phenylephrine (PE) and potassium chloride. After removing the vascular endothelium, its effect disappears. Mechanism studies have shown that its vasodilation effect is related to increasing the content of vascular endothelial NOS and cyclic guanosine monophosphate (cGMP). These findings show that echinacoside has an endothelium-dependent vasodilation effect on mouse aortic rings. Phenylethanol glycoside compounds kankanoside F, kankanose, verbascoside and cistanoside F also have vasodilator effects.

Pic: Cistanche benefits

Neurotoxic injury

This paper first studied the effect of HBOT on the peripheral nerve disorder caused by high dose of antifungal and antigenic drug chloroquinolol in rabbits. The damage of myelin sheath and axon was obvious after the administration of chloroquinolone, and the degree of damage of HBOT decreased.

In another study, the effect of HBOT on streptomycin induced diabetic neuropathy was investigated and the results showed that HBOT could partially reverse chronic diabetic neuropathy. In contrast, Aydin did not find any beneficial effect of HBOT on nerve regeneration in patients with early-stage diabetes. As for the protective effect of HBOT after severe carbon monoxide neuropoisoning, it was found that HBOT could not effectively prevent the neurological sequelae after severe carbon monoxide neuropoisoning in mice.

The last group of studies showed that echinoside in cistanche can significantly increase the total protein content and total antioxidant capacity of brain tissue, litenin can improve cell survival, reduce cell apoptosis and production of reactive oxygen species, tubularin B and echinoside can protect tumor necrosis faction-induced apoptosis.

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Conclusion

In recent years, HBOT has attracted wide attention due to its biological characteristics. As a treatment option, the neuroprotective effect of HBOT has been demonstrated by numerous preclinical in vivo and in vitro studies. These beneficial effects are mainly attributed to antioxidant, anti-inflammatory and anti-apoptotic properties, in addition to improving oxygen supply and neural metabolism and stimulating au tophagy. The evidence presented in this review suggests that HBOT and cistanche tubularis have the potential to treat and prevent various neurological injuries. At the same time, due to the limited data on the neuroprotective effect of HBOT on humans, new clinical trials on the neuroprotective effect of HBOT and its possible mechanism, as well as the course and dose of HBOT are needed.

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