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ObjectiveTo investigate the promotional effect of astragaloside on the repair and healing of chronic non-healing wounds and its mechanism. MethodA total of 60 male SD rats were constructed with full-layer skin defect wounds on the back， and except for the control （Con） group， the rest were constructed with non-healing wounds， which were then randomly divided into the sham-operation （sham） group， the low-dose astragaloside group， the high-dose astragaloside group， the astragaloside + LY294002 ［phosphatidylinositol 3-kinase （PI3K） inhibitor］ group， and the astragaloside + EX527 ［silencing regulatory protein 1 （SIRT1） inhibitor］ group. The percentage of wound area in each group was observed on the 2nd， 4th， 6th， and 8th days after wound molding. Collagen type Ⅰ alpha 1 （COL1A1） and alpha smooth muscle actin （α-SMA） expressions in the wound tissue were detected by immunofluorescence. Hematoxylin and eosin （HE） staining was performed to determine the pathological structure of the wound. The mRNA expression of inflammatory factors in the wound was measured by real-time polymerase chain reaction （Real-time PCR）， and the expression of proteins related to the SIRT1/ nuclear factor （NF）-κB and PI3K/protein kinase B （Akt） signaling pathways in the wound was tested by Western blot. ResultCompared with the sham group， the percentage of postoperative wound area of rats in both low-dose and high-dose astragaloside groups gradually decreased with time， and the efficacy of the high-dose astragaloside group was better. Compared with the Con group， the fluorescence intensity of COL1A1 in wound tissue of the sham group decreased， while the expression of α-SMA increased. The epithelial tissue was severely damaged， with an increase in the thickness， and a large number of inflammatory cells were seen in the infiltration. The mRNA expression of tumor necrosis factor （TNF）-α， interleukin （IL）-1β， IL-6， and inducible nitric oxide synthase （iNOS） was elevated. The protein expression of NF-κB p65， p-PI3K/PI3K， and p-Akt/Akt was elevated， while SIRT1 expression was decreased （P<0.05）. Compared with the sham group， the fluorescence intensity of COL1A1 and α-SMA increased after astragaloside treatment. The number of epithelial cells increased， and the thickness decreased. The inflammatory cells decreased， and the amount of collagen increased. The mRNA expression of TNF-α， IL-1β， IL-6， and iNOS was decreased， and the protein expression of NF-κB p65， p-PI3K/PI3K， and p-Akt/Akt was decreased. SIRT1 was elevated， and the effect was better in the high-dose astragaloside group （P<0.05）. Compared with the high-dose astragaloside group， inhibition of the PI3K/Akt and SIRT1 pathways by LY294002 and EX527 prevented the therapeutic efficacy of astragaloside on chronic non-healing wounds. ConclusionThe topical application of astragaloside significantly promotes the healing of chronic non-healing wounds in rats， and the mechanism may be related to the activation of the PI3K/Akt pathway and the SIRT1/NF-κB pathway.
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Marinesco-Sj?gren syndrome (MSS), also known as hereditary ataxia-dwarf-mental retardation syndrome, is a rare autosomal recessive ataxia syndrome. This article reviews the recent advance in clinic characteristics, pathogenic gene mutation sites, pathogenesis and clinic diagnosis and treatment of MSS, in order to improve clinicians' understanding of the disease and diagnosis and treatment level, and reduce the missed diagnosis and misdiagnosis of the disease.
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Sialidosis is a rare lysosomal storage disease caused by NEU1 gene mutation at 6p21.33. It is characterized by myoclonic, ataxia, epilepsy, and decreased vision. A pair of twins with sialidosis type 1 are reported to enrich clinicians ′ understanding of the disease, so as to improve the diagnosis and treatment. The proband was a 16-year-old male. The main symptom was intermittent limb involuntary trembling for 2 years, with paroxysmal loss of consciousness. Fundus examination showed cherry-red spots. His twin brother had similar symptoms, but the overall performance was mild. Whole exome sequencing results showed that both patients carried compound heterozygous mutations of c.239C>T (p.P80L) and c.803A>G (p.Y268C) in NEU1 gene, which were from their normal phenotype mother and father.
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@#Objective To investigate the protective effect and mechanism of the derivative NIM811 on hypoxia/reoxygenation injury of rat hippocampal neuron (HT22) induced by sodium disulfite (Na2S2O4).Methods The hypoxia/reoxygenation cell model was prepared with mouse HT22 cultured cells.The experiment was divided into normal control group,Na2S2O4 group,Na2S2O4+NIM811 group,and NIM811 group.Cell survival rate was detected by CCK-8,flow cytometry was used to detect apoptosis,mitochondrial membrane potential was detected by JC-1 reagent,calcium ion level in mitochondria was observed by Rhod-2 AM,and reactive oxygen species (ROS) was detected by DCFH-DA method.Results Compared with the Na2S2O4 group,after NIM811 treatment:(1)Cell activity increased by 38% (P<0.01);(2)Apoptosis decreased by 27% (P<0.01);(3)Mitochondrial membrane potential increased (P<0.01);(4)The level of calcium ions in the mitochondria decreased (P<0.01);(5)The level of reactive oxygen species (ROS) decreased (P<0.01).Conclusion NIM811 has a protective effect on the hypoxia/reoxygenation injury of mouse hippocampal neurons caused by Na2S2O4.The mechanism may be related to the maintenance of mitochondrial homeostasis and inhibition of cell apoptosis.NIM811 has therapeutic potential for future clinical treatment of ischemic stroke.
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OBJECTIVE To explor e the characteristics of spectral oscillatory power of resting-state electroencephalography(EEG) in subjective tinnitus patients and to lay the foundation for study of central mechanism of tinnitus.METHODS 31 subjects(15 subjects with subjective tinnitus and 16 age matching healthy subjects) underwent a 128-channel resting-state EEG analyses. After a series of preprocessing, data were segmented into 8 frequency bands, including δ(0.5～3.5 Hz), θ(4～7.5 Hz), α1(8～10 Hz), α2(10～12 Hz), β1(13～18 Hz), β2(18.5～21 Hz), β3(21.5～30 Hz) and γ(30.5～44 Hz). The group differences of spectral power were analyzed by independent t test. Correlation between spectral power of each frequency band and tinnitus subjective symptoms were also analyzed. RESULTS Significant higher spectral power of the α1, β and γ bandwere found in the left and right temporal areas of tinnitus group compared with that of normal group.Tinnitus subjects also had higher spectral powerof the δ and θ band in temporo-parietal areas than that of the normal group. There was no significant difference of spectral power in other frequency bands. Moreover, signif icant positive cor relation were found between tinnitus loudness and spectralpower of right anterior lateral(R=0.66, P =0.007) and right anterior medial(R=0.58, P =0.031) areas. CONCLUSION Tinnitus subjects have higher spectral oscillatory power on right and left temporal lobe and temporo-parietal area. A positive correlation exsit between tinnitus loudness andspectral power of right anterior lateral and medial areas in tinnitus subjects, whichindicate that central reorganizationexsit in tinnitus reorganization andγ band maybe considered as a possible biomarkerforthe tinnitus subjective symptom.