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The term Jingluo, translated as meridian or channel, is a core component of traditional Chinese medicine (TCM) and has played a fundamental role in guiding the clinical practice of acupuncture for thousands of years. However, the essence of the meridian remains elusive and is a source of both confusion and debate for researchers. In this study, a "4D" systemic view on the essence of the meridian, namely substantial, functional, chronological, and cultural dimensions, was proposed based on a review of the ancient medical classics, recent research developments, and results from clinical practice. Previous studies have primarily focused on the substantial dimension of the meridian system, with scant interpretation about its functional domain. Neither systemic data nor evaluations have been adequately documented. Additionally, a limited but increasing number of studies have focused on the chronological and cultural dimensions. More investigations that embody the holistic concept of TCM and integrate the systemic modes and advanced techniques with dominant diseases of TCM need to be performed to obtain a more comprehensive understanding of the essence of meridians. The goal of this study is to yield useful information in understanding the essence of meridians and provide a reference and perspective for further research.
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Acupuncture , Acupuncture Points , Acupuncture Therapy , Medicine, Chinese Traditional , MeridiansABSTRACT
ObjectiveTo investigate the potential mechanism of Xiao Chaihutang （XCHT） in the treatment of Alzheimer's disease （AD） based on network pharmacology and bioinformatics. MethodThe active components of XCHT and corresponding targets were retrieved from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）， and the differentially expressed genes related to AD were searched from Gene Expression Omnibus （GEO）. Thereby， the common targets of XCHT and AD were yielded， followed by Gene Ontology （GO） term enrichment and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis of the common targets. The component-target network and protein–protein interaction （PPI） network were constructed. Furthermore， amyloid β-protein （Aβ）1-40 was used to induce AD in PC12 cells and then the AD cells were intervened with XCHT. Afterward， cell viability was detected by Cell Counting Kit-8 （CCK-8） assay and cell morphology was observed based on 4'，6-diamidino-2-phenylindole （DAPI） staining. Cell membrane potential was determined and apoptosis was detected by flow cytometry， and cellular immunofluorescence detects the expression of B-cell lymphoma-2 （Bcl-2）/Bcl-2-related X protein （Bax）. Moreover， immunofluorescence assay was performed. ResultA total of 190 active components and 41 anti-AD targets of XCHT were screened out. The key components included mairin， quercetin， berberine， protoporphyrin， 24-ethylcholest-4-en-3-one， and β-D-ribofuranoside， and the core targets were sigma non-opioid intracellular receptor 1 （SIGMAR1）， checkpoint kinase 1 （CHEK1）， protein tyrosine phosphatase non-receptor type 6 （PTPN6）， protein kinase C（PRKCH）， inhibitor of nuclear factor kappa B kinase subunit beta （IKBKB）， cathepsin D （CTSD）， cysteine aspartate protease-3 （Caspase-3）， Bax， and Bcl-2-like protein 1 （Bcl-2L1）. The anti-AD targets of XCHT were involved in 302 GO terms （P < 0.05）， particularly the regulation of neuronal cell apoptosis， and 73 KEGG pathways （P<0.05）. The major pathways and biological processes included the apoptosis pathway， virus infection pathway， lipid and atherosclerosis pathway， and cancer-related pathways. In the in vitro experiment， the model group demonstrated the decrease in cell survival rate （P<0.05）， increase in apoptosis rate （P<0.05）， and down-regulation of mitochondrial membrane potential and Bcl-2/Bax ratio compared with the blank control. Compared with the model group， XCFT group showed the increase in cell survival rate （P<0.05）， decrease in apoptosis rate （P<0.05）， and up-regulation of mitochondrial membrane potential and Bcl-2/Bax ratio. ConclusionBased on network pharmacology， this study reveals the multi-component， multi-target， and multi-pathway characteristics of XCHT in the treatment of AD， laying a foundation for further research on the material basis and mechanism of this prescription.
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Background Rigid gas permeable (RGP) contact lens,as a kind of new correction of refraction error,has been wildly used,but whether it will cause eye optical system of the change and influence on the visual acuity is unclear.Objective Present study was to evaluate and compare the visual quality of low to moderate myopia following wearing of RGP contact lens and spectacles.Methods Sixty-eight eyes of 35 subjects with low or mediate myopia were included in this study.Wave-front aberrations and visual acuities under the different contrasts (10％,30％,40％,52％,76％,92％) in the light or dark environment were examined before and 3 months after wearing of RGP corneal contact lens.These parameters were compared with those after wearing of spectacles with paired t test.Results The best corrected visual acuity (BCVA) was improved significantly from 0.94±0.10 to 1.26±0.03 3 months after wearing of RGP corneal contact lens (t=-9.266,P=0.000).After fitting of RGP corneal contact lens,the total higher order wave-front aberrations,the 3rd and 4th order aberrations were significantly declined in comparison with those of before fitting (total:t=4.683,P=0.000;RMS3:t=4.656,P=0.000;RMS4:t=3.929,P=0.000).However,no significant differences were detected in the 5th and 6th order aberrations between RGP corneal contact lens fitting and spectacles wearing (RMS5:t=1.766,P=0.083 ;RMS6:t=1.150,P=0.256).In both bright and dark environments,BCVA values were much better in the eyes with RGP corneal contact lens wearing than that in the eyes with spectacles wearing (all P＜0.05).The BCVA was always reduced with the decline of contrast level whether bright or dark backgrounds both in RGP corneal contact lens wearing eyes and spectacles wearing eyes.Conclusions Wearing of RGP corneal contact lens provides better visual quality for low to moderate myopia than the spectacles wearing.
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Background Leber hereditary optic neuropathy (LHON)is a mitochondrial DNA (mtDNA)hereditary disease,so it is significant to understand the influence of DNA mutation on the occurrence of LHON.Objective This survey was to evaluate the role of mtDNA mutation in the development of LHON.Methods This survey study was approved by the Ethic Committee of Wuhan General Hospital of Guangzhou Military Command and written informed consent was obtained from each subject before the relative medial examination.Seventy-two matrilineal relatives from a family with LHON were collected for a pedigree analysis and mutation screening.Regular eye examination was performed on 11 patients,13 mutant gene carriers and 49 individuals with normal phenotype,and the degree of visual damage was graded as follows: ＞0.3 was normal,0.1-0.3 was mild damage,＜0.05-0.1 was moderate damage,＜0.02-0.05 was severe damage and ＜0.01 was very severe damage.Clinical characteristics of LHON was evaluated.The periphery blood sample of 2-4 ml was collected from individuals to separate the mononuclear cells,and the mtDNA was extracted by modified high salt method.MtDNA was amplified by PCR and the mutation loci was sequenced.Results PCR amplification product sequencing of mutant gene showed that both G11778A and T14502C mutations were detected in 24 of 72 matrilineal relatives,but only 11 of 24 carriers developed LHON.No abnormal clinical findings were seen in the 13 carriers,showing a less 50％ penetrance in this family.There was no G11778A or/and T14502C mutation in the normal phenotype individuals of this family.The onset age for vision impairment in 11 affected matrilineal relatives varied from 8 to 50 years old,with the mean age of 24.36 years old,showing a significantly lower age than that of the 13 carriers (5-72 years old,mean 40.38 years old) (t =2.102,P=0.049).Conclusions This study suggests that the Gl1778A and T14502C mutation in mitochondrial DNA is one of causes in the development of LHON.The primary G11778A mutation together with T14502C mutation in mtDNA is a factor for the occurrence of LHON,hut it is not sufficient to the development of LHON.An effective “second hit” process will play an inducing role for LHON.
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<p><b>OBJECTIVE</b>To observe the effect of exendin-4 on cardiomyocyte apoptosis in the early stage after scald injury in rats and explore the mechanisms.</p><p><b>METHODS</b>Fifty-four healthy adult SD rats were randomly divided into normal control group (n=6), scald group (n=24) and scald with exendin-4 treatment group (n=24). In the latter two groups, the rats were subjected to 30% TBSA full-thickness scald burns on the back, and Parkland formula was used for determining the resuscitation fluid volume. In exendin-4 treatment group, the rats received intraperitoneal injection of 5 µg/kg exendin-4 after the scald. Apoptosis of the cardiomyocytes from the left ventricle was determined by TUNEL assay and the activity of caspase-3 in the myocardium was assessed.</p><p><b>RESULTS</b>In the scald group, the apoptotic index of the cardiomyocytes was increased at 6 h post-burn, reaching the peak level at 12 h, and maintained a significantly higher level than that in the normal control at 48 h (P<0.05). Myocardial caspase-3 activity in the scald group was increased at 6 h post-burn and reached the peak at 12 h, still maintaining a high levels at 24 h (P<0.05). In exendin-4 treatment group, the apoptotic index of the cardiomyocytes was significantly lower than that in the scald group at 6, 12, 24 and 48 h post-burn (P<0.05), and so was the caspase-3 activity at 6, 12 and 48 h (P<0.05). A significant positive correlation was found between the apoptotic index of the cardiomyocytes and myocardial caspase-3 activity in the rats (P<0.05).</p><p><b>CONCLUSION</b>Exdendin-4 can inhibit rat cardiomyocyte apoptosis early after scald injury possibly by suppressing caspase-3 activity in the myocardium.</p>