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Objective:To compare the effects of different test meals on postprandial triglycerides and to optimize the standard meal composition and the blood sampling protocol for the oral fat tolerance test.Methods:This study is a prospective, open-label, randomized, cross-over trial. In March 2023, 36 volunteers were recruited in Hebei General Hospital. They underwent a health examination and oral glucose tolerance test. Twenty-six healthy volunteers(11 males and 15 females) were included in this study, with an average age of(39.08±4.56) years. Each volunteer received 75 g protein meal, 75 g fat meal, 700 kcal fixed-calorie high-fat mixed meal, and a high-fat mixed meal with energy adjusted based on 10 kcal/kg body weight. A one-week washout period of regular diet was applied before each trial. Blood was collected at fasting status and 1, 2, 3, 4, 5, and 6 hours after a meal to detect serum triglycerides, total cholesterol, low density lipoprotein-cholesterol(LDL-C), high density lipoprotein-cholesterol(HDL-C), glucose, and insulin. The variations of postprandial metabolic indicators over time following the consumption of different test meals were analyzed. The disparities in postprandial metabolic responses between the two types of mixed meals were compared.Results:The protein meal, fat meal, fixed-calorie high-fat mixed meal, and adjusted-calorie high-fat mixed meal resulted in postprandial triglyceride increases of 22.45%, 115.40%, 77.14%, and 63.63%, and insulin increase of 560.43%, 85.69%, 554.18%, and 598.97%, respectively, and with reductions in total cholesterol, LDL-C, and HDL-C ranging from 5.64%-21.81%, respectively. The blood glucose changed slightly. Changes in metabolic indicators mainly occured within 4 hours. The comparison of the characteristics of postprandial triglycerides between the two high-fat mixed meals showed no statistically significant differences( P>0.05). Conclusion:A standardize protocol with a 700 kcal fixed-calorie high-fat mixed meal as test meal, and blood lipid levels measured at fasting and at 1, 2, 3, and 4 hours after consumption, can serve as an optimized approach for oral fat tolerance test.
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AIM: To explore retinal microvascular changes in migraine patients using meta-analysis.METHODS: The National Library of Medicine PubMed, Embase, and Cochrane Library were searched to find relevant studies, and the search period was from the creation of database to June 2023. Two investigators independently screened the literatures, extracted data, and evaluated the quality of included studies using the NOS scale. STATA15.0 was used for Meta-analysis and publication bias evaluation, sensitivity analysis was performed for results with large heterogeneity, and the funnel plot and Egger were used to assess the publication bias of the literature.RESULTS:A total of 12 studies, including 217 patients(252 eyes)with migraine with aura(MA), 283 patients(388 eyes)with migraine without aura(MO), and 374 healthy individuals(479 eyes), were included in this Meta-analysis. Several optical coherence tomography angiography(OCTA)indicators, including foveal avascular zone(FAZ)macular or optic disc perfusion density were compared and analyzed. The Meta-analysis results showed that compared with healthy controls, patients with MA had a significant increase in FAZ area and perimeter, a significant decrease in perfusion density of the macular deep capillary plexus(mDCP)except for the fovea, and a significant decrease in perfusion density of the radial peripapillary capillaries(RPC)around the optic disc; the FAZ parameters were significantly increased in MO, while the differences in perfusion density of the macular superficial capillary plexus(mSCP), mDCP and RPC were not statistically significant, except for the perfusion density in the parafovea mDCP.CONCLUSIONS: Both MA and MO patients had an enlarged FAZ area, patients with MA had a significant decrease in mDCP perfusion density, and migraine patients had some degree of retinal ischemia.
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AIM:To systematically evaluate the changes in retinal and choroidal thickness in patients with internal carotid artery stenosis by using optical coherence tomography(OCT)through Meta-analysis.METHODS: Literatures on the measurement of retinal and choroidal structure in patients with internal carotid artery stenosis by using OCT from CNKI, VIP, WF, PubMed, the Cochrane Library, SinoMed, and Embase databases were searched for relevant studies. The retrieval time was from the establishment of the databases to January 2024. In addition, quality of the included literatures was assessed by the Newtle-Ottawa scale(NOS), and RevMan 5.4.1 and Stata 16.0 were used for statistical analysis.RESULTS: A total of 17 articles(including 18 studies)were included, and the Meta-analysis results showed that, patients with internal carotid artery stenosis had significantly thinner peripapillary retinal nerve fiber layer(pRNFL), ganglion cell complex(GCC), center macular thickness(CMT), and subfoveal choroidal thickness(SFCT)than the healthy control group(age matched normal population). The pRNFL and SFCT of the ipsilateral eye in patients with internal carotid artery stenosis become thinner compared with the contralateral eye.CONCLUSION:To a certain extent, the morphological structure of the retina and choroid can be altered by stenosis of the internal carotid artery. OCT can non-invasively detect the microstructural changes of the retina and choroid in patients with internal carotid artery stenosis, and can be used for the evaluation of internal carotid artery stenosis.
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Objective @#To investigate the effect of Arginine Vasopressin (AVP) on the median preoptic glutamatergic (MnPOVglut2 ) neurons and its mechanism．@*Methods @#Brain slices were prepared from male Vglut2-tdTomato mice．MnPOVglut2 neurons expressing red fluorescent protein were located by using fluorescence microscope．Wholecell patch clamp technique was used to observe the effect of AVP on the firing frequency of MnPOVglut2 neurons，the effect of synaptic transmission blockers ( STBs) on the AVP-induced change in the firing frequency of MnPOVglut2 neurons，and the effect of AVP V1a receptor antagonist on the AVP-induced change in the firing frequency of MnPOVglut2 neurons. @*Results@#The mean firing frequency of MnPOVglut2 neurons increased during perfusion with artificial cerebrospinal fluid (ACSF) and AVP compared with that during perfusion with ACSF (P＜0. 01) ，indicating that AVP excited the MnPOVglut2 neurons．The mean firing frequency of MnPOVglut2 neurons still increased during perfusion with ACSF，STBs，and AVP compared with that during perfusion with ACSF and STBs (P＜0. 001) ; moreover，the magnitude of AVP-induced increase in firing frequency didn't change significantly during perfusion with ACSF，STBs，and AVP compared with that during perfusion with ACSF and AVP (P ＞0. 05 ) ，suggesting that AVP excited the MnPOVglut2 neurons directly in a postsynaptic manner．The magnitude of AVP-induced increase in the firing frequency of MnPOVglut2 neurons declined during perfusion with ACSF，STBs，AVP，and V1areceptor antagonist compared with that during perfusion with ACSF，STBs，and AVP (P＜0. 01) ，suggesting that AVP excited MnPOVglut2 neurons directly via V1a receptor．@*Conclusion @#AVP can excite MnPOVglut2 neurons via V1areceptor directly in a postsynaptic manner．This study reveals the molecular marker of MnPO neurons which AVP act on.
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AIM: To explore schisandrin B (Sch B) pretreatment reduces intestinal ischemia reperfusion injury (IIRI) through inhibiting apoptosis by activation of Nrf2/HO-1 signing pathway in mice by network pharmacology and in vivo experiment. METHODS: (1) The targets of Sch B and IIRI were searched from online databases, Drawing Venn diagram to obtain the common target of them. Cytoscape software was imported to construct the protein-protein interaction (PPI) network to establish the "Drugs-Disease-core target gene" network. The mechanism of Sch B against IIRI was predicted through GO and KEGG enrichment analysis. (2) Thirty-six C57BL/6J mice were randomly divided into six groups (n = 6). The model of IIRI was established in four groups except the sham operation group. Three of the groups were pretreated with Sch B, Nrf2 inhibitor ML385, and Sch B + ML385, respectively. After the experiment, intestinal tissue samples were taken for HE staining, Chiu ' s score, apoptosis staining, immunohistochemistry (IHC), and immunoblotting (Western blot). RESULTS: A total of 412 Sch B related tar- gets, 2 166 IIRI related targets and 153 common targets were screened out through network pharmacology. There were 88 "Sch B-IIRI-core target gene" included NFE2L2 (Nrf2), HMOX1 (HO-1), BCL2, CASP3 (caspase 3), and so on. KEGG enrichment analysis screened 163 related pathways, apoptosis pathway ranked high showing that the pathway may play a key role in the treatment of IIRI by Sch B. The animal experiment had shown that Sch B reduced the Chiu's score and apoptotic while upregulating Nrf2, HO-1, Bcl-2 protein expression levels and Bcl-2/Bax, downregulating Bax, and cleaved caspase-3 expression levels, thereby reducing IIRI in mice, and that Nrf2 inhibitor ML385 reversed this process (P < 0.05). CONCLUSION: This study reveals that Sch B has the characteristics of multi-target and multi-pathway in the reduction of IIRI, and Sch B can reduce IIRI through inhibiting apoptosis by activation of Nrf2/ HO-1 pathway.
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AIM: To verify the role of tetramethylpyrazine (TMP) in intestinal ischemia-reperfusion (I/ R) injury and its relationship with pyroptosis. METHODS: Thirty-six healthy SPF male C57BL / 6 mice, 8-12 weeks old, weighing 20-25 g, were divided into six groups randomized by table of random number (n = 6/group): Sham group (S1 group)Ischemia/reperfusion group (I/R1 group), I/R + TMP treatment group: 15 mg/kg (T15 group), 30 mg/kg (T30 group), 60 mg/kg (T60-1 group), 120 mg/kg (T120 group). In experiment 2, thirty healthy SPF male C57BL/6 mice were divided into five groups (n = 6/group): Sham group (S2 group), I/R group (I/ R2 group), I/R + dimethyl sulphoxide (DMSO) group (DMSO group), I/R + TMP (60 mg/kg) group (T60-2 group), and I/R + DMSO + TMP (60 mg/kg) + Nigericin sodium salt (NSS) group (T60+NSS group). I/R-induced intestinal injury was established by clamping the superior mesenteric artery for 45 minutes, followed by 120 minutes of reperfusion, while the sham group mice underwent isolation of superior mesenteric artery without clamping. An NLRP3 agonist NSS was dissolved in DMSO, was intraperitoneally injected (4 mg/kg) 60 minutes before ischemia. And DMSO group mice were intraperitoneally administered with corresponding DMSO. Different TMP dosage groups and T60+NSS group mice were intraperitoneally administered with TMP 30 minutes before ischemia. IL-1β and IL-18 concentrations in the intestine were measured at 120 minutes after reperfusion by ELISA. The pathological changes of the sections were observed by optical microscope, and the intestinal mucosal injury was evaluated by Chiu's score grading. Western blot was used to detect NLRP3, Caspase-1, and GSDMD in intestinal tissue. RESULTS: Statistically significant increase of Chiu's score, IL-1β, IL-18 concentrations in the I/R1 group were found as compared with S1 group (P<0.05). And compared with I / R1 group, Chiu's score and IL-1β, IL-18 concentrations in the T60-1, T120 groups were reduced (P<0.05). Moreover, Chiu's score in the T120 group was lower than that in the T60 group (P<0.05). We found a statistically significant increase of Chiu's score and IL-1β, IL-18 concentrations and the expression of NLRP3, GSDMD, caspase-1 in the I/R group (P<0.05) as compared with S2 group. Compared with I / R2 group, Chiu's score, IL-1β, IL-18 concentrations and NLRP3, GSDMD, caspase-1 expression in the T60-2 group was reduced (P<0.05). Compared with T60-2 group, Chiu's score, IL-1β, IL-18 concentrations and NLRP3, GSDMD, caspase-1 expression in the T60 + NSS group were upregulated (P<0.05). CONCLUSION: The protective effect of TMP against intestinal I / R injury was dose-dependent. And TMP can decrease pyroptosis mainly by inhibiting the activation of the NLRP3 inflammasome.
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In the early stage of diabetes retinopathy(DR),the change in the molecular level is often earlier than chan-ges in retinal microvessels.Under the chronic high-glucose environment,oxidative stress,epigenetic changes and other mechanisms cause retinal mitochondrial DNA(mtDNA)damage,affect the transcription process of mtDNA coding genes,and damage the electronic transport chain,leading to a vicious cycle of free radicals,which accelerates the apoptosis of retinal capillary pericytes and endothelial cells,leads to retinal microcirculation dysfunction,and cause DR.This paper will review the epigenetic changes,oxidative stress,damage to replication and repair system,gene mutation and other aspects,in order to elaborate on the research progress of retinal mtDNA damage in the pathogenesis of DR.
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Objective:To evaluate the role of histone deacetylase 6 (HDAC6) in reduction of intestinal ischemia-reperfusion (I/R) injury by sodium butyrate in mice.Methods:Twenty-four SPF healthy adult male C57BL/6 mice, aged 8-10 weeks, weighing 22-25 g, were divided into 4 groups ( n=6 each) by the random number table method: sham operation group (S group), intestinal I/R group (I/R group), intestinal I/R + sodium butyrate group (I/R+ SB group), and intestinal I/R + ITSA-1+ sodium butyrate group (I/R+ I+ SB group). The model of intestinal I/R injury was established by clipping superior mesenteric artery for 45 min followed by 120 min of reperfusion in anesthetized animals.In I/R+ I+ SB group, the HDACs activator ITSA-1 0.5 mg/kg was intraperitoneally injected at 6, 3 and 1 days before ischemia.Sodium butyrate 500 mg/kg was given by intragastric administration every day one week before ischemia in I/R+ SB group and I/R+ I+ SB group, and the equal volume of normal saline was given in S group and I/R group.At 120 min of reperfusion, the mice were sacrificed and their small intestine tissues were obtained.The levels of diamine oxidase (DAO) in serum and intestinal tissues were detected by enzyme-linked immunosorbent assay.The pathological changes of small intestinal tissues were observed with a light microscope, and intestinal damage was assessed and scored according to Chiu.The expression of microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ), P62 and HDAC6 was determined by Western blot.The contents of histone H3 (H3) and acetylated histone H3 (Ac-H3) in small intestinal tissues were determined by enzyme-linked immunosorbent assay. Results:Compared with S group, the Chiu′s score, levels of DAO in serum and small intestinal tissues were significantly increased, the expression of LC3 Ⅱ and HDAC6 was up-regulated, P62 expression was down-regulated, H3 content was increased, and AC-H3 content was decreased in I/R group ( P<0.05). Compared with I/R group, the Chiu′s score, levels of DAO in serum and small intestinal tissues were significantly decreased, the expression of LC3 Ⅱ and HDAC6 was down-regulated, P62 expression was up-regulated, H3 content was decreased, and AC-H3 content was increased in I/R+ SB group ( P<0.05). Compared with I/R+ SB group, the Chiu′s score and levels of DAO in serum and small intestinal tissues were significantly increased, the expression of LC3 Ⅱ and HDAC6 was up-regulated, P62 expression was down-regulated, H3 content was increased, and AC-H3 content was decreased in I/R+ I+ SB group ( P<0.05). Conclusions:Sodium butyrate can alleviate intestinal I/R injury by inhibition of HDAC6 activity in mice, and the mechanism may be related to inhibition of autophagy and promotion of H3 acetylation.
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Objective:To evaluate the role of histone deacetylase (HDAC) in sodium butyrate-induced reduction of intestinal ischemia-reperfusion (I/R) injury in mice and the relationship with oxidative stress and cell apoptosis.Methods:Twenty-four SPF healthy male C57BL mice, aged 6-8 weeks, weighing 22-25 g, were divided into 4 groups ( n=6 each) according to the random number table method: sham operation group (S group), intestinal I/R group (IR group), intestinal I/R+ sodium butyrate group (IN group) and intestinal I/R+ ITSA-1+ sodium butyrate group (INI group). In IR, IN and INI groups, the superior mesenteric artery was clamped for 45 min, followed by reperfusion for 2 h to prepare the model of intestinal I/R injury, while the superior mesenteric artery was only isolated without ligation in S group.One week before preparation of the model, sodium butyrate 500 mg/kg was intragastrically administered once a day in IN group and INI group, the HDAC activator ITSA-1 0.5 mg/kg was intraperitoneally injected three times a week in INI group, and the equal volume of normal saline was given instead in the other groups.The mice were sacrificed at 2 h of reperfusion and small intestinal tissues were obtained for microscopic examination of the pathological changes which were assessed using Chiu′s score and for determination of the content of MDA (by enzyme-linked immunosorbent assay) and expression of cleaved caspase-3 (by Western blot). Results:Compared with S group, Chiu′s score was significantly increased, and the expression of cleaved caspase-3 was up-regulated in IR, IN and INI groups, the content of MDA in small intestinal tissues was significantly increased in IR and INI groups ( P<0.05). Compared with IR group, Chiu′s score was significantly decreased in IN and INI groups, and the content of MDA was significantly decreased, and the expression of cleaved caspase-3 was down-regulated in IN group ( P<0.05). Compared with IN group, Chiu′s score and content of MDA were significantly increased, and the expression of cleaved caspase-3 was up-regulated in INI group ( P<0.05). Conclusions:HDAC is involved in sodium butyrate-induced reduction of intestinal I/R injury in mice, which is related to the inhibition of oxidative stress and cell apoptosis.
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lrisin is an endogenous secreted muscle factor, Which not only plays a certain clinical application value in a variety of metabolic diseases, cardiovascular and cerebrovascular diseases, neurological diseases, tumors and other diseases, but also affects the occurrence and development of organ ischemia/reperfusion injury. ln this paper, the role and mechanism of irisin in organ ischemia/reperfusion injury Were summarized, aiming to provide neW ideas for prevention and treatment of organ ischemia/reperfusion injury.
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Short-chain fatty acids (SCFAs) are organic acids with no more than 6 carbon atoms produced during the anaerobic fermentation of dietary fiber in the intestinal tract, which can regulate intestinal flora, repair intestinal mucosal barrier, and reduce intestinal injury.Ischemia-reperfusion injury (IRI) is the main cause of various diseases, and the pathological mechanisms involved are intricate, among which inflammation, oxidative stress, apoptosis and autophagy are the most common. According to current studies, SCFAs can affect the occurrence and development of IRI in various organs by regulating different cell signal transduction. In this paper, the role and mechanism of SCFAs in alleviating tissue and organ ischemia-reperfusion injury were preliminarily summarized, providing theoretical reference for clinical prevention and treatment of IRI.
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Butyrate is the main product of colonic and cecal microbiota in the fermentation of dietary fiber and some amino acids, which can reduce intestinal inflammation, regulate the balance of intestinal flora, and improve intestinal mucosal barrier. In recent years, a large number of studies at home and abroad have shown that butyrate plays a role in intestinal diseases such as inflammatory bowel disease, irritable bowel syndrome, intestinal ischemia-reperfusion injury, colorectal cancer and short bowel syndrome. This article reviewed the research progress on role and mechanism of butyrate in intestinal diseases.
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Objective To discuss the clinical application and value of dual-source spiral CT enhanced scan and multiplanar reformatting ( MPR) in the diagnosis of gastric cancer. Methods The 335 patients with gastric cancer who conducted dual-source spiral CT enhanced scan of upper abdomen under the hypotonic state before the definite pathological diagnosis were retrospectively analyzed,and had multi-di-mensional multiplanar reconstruction for the enhanced thin-section CT data by the multiplanar reformatting technique. Results Of 335 ca-ses,288 cases were detected by simple axial data,the detection rate was 86. 0%,320 cases were detected by MPR,the detection rate was 95. 5%,the differences were statistically significant (P<0. 05). The overall accuracy rate of Preoperative T staging by conventional axial and MPR images were 78. 3% and 89. 1% respectively, the difference was statistically significant. The overall accuracy rate of preoperative N staging by two methods were 73. 6% and 82. 3%,respectively,the difference was not significant. Conclusion Application of dual source spiral CT multiplanar reconstruction can significantly improve the detection rate of gastric cancer,and the average accuracy rate of preopera-tive TNM staging for gastric cancer is 84. 6%.
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[ ABSTRACT] AIM: To discuss the relevance between the pathogenesis of diabetic gastroparesis and the large-conductance calcium-activated potassium channels ( BKCa ) in gastric smooth muscle cells.METHODS:The SD rats were randomly divided into control group and model group.The gastric smooth muscle cells of the SD rats were enzymatically iso-lated in a low calcium solution containing papain.The current was recorded by patch clamp single channel recording tech-nique.The expression of KCNMA and KCNMB1 were observed by the method of immunohistochemistry.RESULTS:The value of BKCa single channel conductance was (220.10 ±10.90) pS;the channels had distinct voltage dependent and cal-cium dependent characteristics.In outside-out patch (Vm =+30 mV), the activation of BKCa was blocked by 200 nmol/L IbTX completely.Compared with control group, the open probability and amplitude of current in model group significant-ly increased, while the mean open time and mean close time significantly decreased.Compared with control group, the ex-pression of KCNMB1 in model group was significantly increased.CONCLUSION: Up-regulation of β1-subunit and in-crease in BKCa functional activities may be associated with diabetes gastroparesis in rats.