protective

摘要： Myelomeningocele(MMC)is a severe form of spinal dysraphism.Due to the failure of neural tube closure during early embryonic development,the affected part of the spinal cord is left open like a book at the back of the affected child.This malformed part of the spinal cord is not covered by its protective mesodermal and ectodermal derived layers.Consequently,the exposed neural tissue(i.e.,the neural placode)is prone to injuryduring further intra-uterine development.

摘要： Parkinson's disease(PD)is the most frequent movement disorder and the second most prevalent age-related neurodegenerative disease(ND)worldwide.From the clinical point of view,it is characterized by severe motor complications,including uncontrollable resting tremors,rigidity,bradykinesia,and postural instability.

摘要： Neurodegeneration of the central nervous system(CNS)underscores many of humanity’s most debilitating diseases,including Alzheimer’s disease,Parkinson’s disease,and multiple sclerosis.Recently,the nitric oxide-guanylate cyclase-cyclic guanosine monophosphate(NO-GC-cGMP)signaling pathway has gained traction as a neuroprotective pathway in the CNS.As an extension of the CNS,the retina is also susceptible to neurodegeneration with age.The most prevalent optic neuropathy is glaucoma,the world’s leading cause of irreversible blindness,predicted to affect more than 112 million people worldwide by 2040(Calkins,2021).In glaucoma,vision loss occurs due to the progressive degeneration of retinal ganglion cells(RGCs),the output neurons of the retina,along with their axons which form the optic nerve(Wareham et al.,2022).Degeneration of RGCs leads to a characteristic pattern of scotopic visual field deficiencies that spread from one retinotopic sector to the next(Elze et al.,2015).Visual deficits are linked to increasing age and the sensitivity of RGCs to intraocular pressure(Calkins,2021).

摘要： Hypoxic-ischemic encephalopathy(HIE)has an incidence of 1-3 in 1000 term births in high-income countries(Zhou et al.,2020).The standard treatment for these infants is therapeutic hypothermia.Although therapeutic hypothermia significantly reduces the risk of death and disability for infants with HIE,it is still only partially protective as up to 45%of infants still develop disability despite treatment(Zhou et al.,2020).The current therapeutic hypothermia protocol is optimal for widespread use in infants with moderate to severe HIE.However,it is possible that a more tailored approach for individual babies,including stratification of the cooling regimen for the severity of HIE and the identification of reliable biomarkers to guide treatment,may improve efficacy in the future.

摘要： Due to their intense electrical activity,neurons have high energy demands.This requirement makes them particularly sensitive to mitochondrial dysfunction.Like all eukaryotic cells,neurons have intrinsic mechanisms to mitigate the impact of mitochondrial dysfunction and its consequent production of toxic substances.Among such(neuro)protective mechanisms,mitochondrial autophagy(mitophagy)is responsible for the removal of dysfunctional mitochondria.Pathological inhibition of mitophagy,together with insufficient mitochondrial activity,results in a shortage of adenosine triphosphate(ATP)and the accumulation of reactive oxygen species(ROS)(Simmons et al.,2020).

摘要： The earliest use of Lycium barbarum L.(Goji fruits)as a medicinal plant was at around 2,300 years ago,and nowadays it is used as a medicinal food(Figure 1)[1,2].There have been some reports on the antifertility effects and fertility-promoting or aphrodisiac effects[3-5].The famous Chinese herbalist Li Shizhen first recorded the pro-fertility efficacy of Lycium barbarum L.in Compendium of Materia Medica in the 16th century[6].Lycium barbarum L.also has many other effects,such as the antioxidant function,anti-cytotoxicity,anti-fatty acid toxicity,neuroprotective and anticancer effects,and so on[7].Lycium barbarum L.is rich in vitamins,zeaxanthin,carotenoid and other ingredients[8].

摘要： Alzheimer’s disease(AD)is the most common cause of dementia in the elderly.Unfortunately,there are no effective therapies currently available for prevention and treatment of AD.As it is clear now,the etiology of AD is multifactorial and complex.This means that development of AD is linked to multiple mechanisms or signaling pathways and that a single-target therapy for AD is likely insufficient to achieve therapeutic goals.Therefore,an ideal therapy for AD should be able to modify the disease through multiple signaling pathways.2-Arachidonoylglycerol(2-AG)is an endogenous cannabinoid(endocannabinoid)displayinganti-inflammator y a n d neuroprotective properties,while its metabolites are arachidonic acid(AA)and AA-derived prostaglandins and leukotrienes,which are proinflammatory and neurotoxic(Figure 1).

摘要： Bacterial infection is a common finding in patients,who develop medication-related osteonecrosis of the jaw(MRONJ)by the longterm and/or high-dose use of anti-resorptive agents such as bisphosphonate(BPs).However,pathological role of bacteria in MRONJ development at the early stage remains controversial.Here,we demonstrated that commensal microbiota protects against MRONJ development in the pulp-exposed periapical periodontitis mouse model.C57/BL6 female mice were treated with intragastric broadspectrum antibiotics for 1 week.Zoledronic acid(ZOL)through intravenous injection and antibiotics in drinking water were administered for throughout the experiment.Pulp was exposed on the left maxillary first molar,then the mice were left for 5 weeks after which bilateral maxillary first molar was extracted and mice were left for additional 3 weeks to heal.All mice were harvested,and cecum,maxilla,and femurs were collected.ONJ development was assessed usingμCT and histologic analyses.When antibiotic was treated in mice,these mice had no weight changes,but developed significantly enlarged ceca compared to the control group(CTL mice).Periapical bone resorption prior to the tooth extraction was similarly prevented when treated with antibiotics,which was confirmed by decreased osteoclasts and inflammation.ZOL treatment with pulp exposure significantly increased bone necrosis as determined by empty lacunae and necrotic bone amount.Furthermore,antibiotics treatment could further exacerbate bone necrosis,with increased osteoclast number.Our findings suggest that the commensal microbiome may play protective role,rather than pathological role,in the early stages of MRONJ development.

摘要： Background L-Carnitine(LC)is an endogenous molecule which is biosynthesized from L-lysine and L-methionine and involved in fatty acid metabolism.LC can be found in foods,but it is especially abundant in beef,lamb,fish,poultry and milk.LC transports the chains of fatty acids into the mitochondrial matrix,thus allowing the cells to break down fat and get energy from the stored fat reserves[1].Carnitine is a conditionally essential nutrient.It is a vital factor for energy production and fatty acid metabolism.Carnitine deficiencies can be associated with genetic mutations of carnitine transporters or chronic diseases(liver and kidney disease).Aberrations of carnitine regulation with subsequent carnitine deficiency is associated with diabetes mellitus,sepsis,cardiomyopathy,protein-energy malnutrition,cirrhosis,various endocrine disorders and with aging.It has been found that nutritional supplementation of LC might be helpful for uremic patients,as a complementary therapy for neuropathic pain,or in diabetic patients.Still,it is a life-saving therapy in primary carnitine deficiency.LC supplementation(LCS)is also investigated in Alzheimer's disease and hepatic encephalopathy.It has been observed that topical application of LC in dry eye syndrome is osmoprotective and it also modulates immune and inflammatory responses.There is some evidence in the available scientific literature supporting that LCS may be beneficial in cardiovascular diseases and obesity.There is also some evidence showing the association improved glucose intolerance and total energy expenditure[2].

摘要： This study aimed to investigate the neurotoxicity induced by trichloroacetic acid(TCA)and the possible protective mechanisms of boron(B).Mouse BV2 cells were treated with TCA(0,0.39,0.78,1.56,3.12,6.25,or 12.5 mmol/L)and B(0,7.8,15.6,31.25,62.5,125,500,or 1,000 mmol/L)for 3 h and 24 h,respectively.Then,reactive oxygen species,and supernatant proinflammatory cytokine and protein levels were analyzed after 24 h of combined exposure.Beyond the dose-dependent decrease in the cellular viability,it clearly increased after B supplementation(P<0.05).Moreover,B decreased oxidative damage,and significantly down-regulated IL-6 levels and up-regulated TNF-βproduction(P<0.05).B also decreased apoptosis via the p53 pathway.The present findings indicated that TCA may induce oxidative damage,whereas B mitigates these adverse effects by decreasing cell apoptosis.