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OBJECTIVE To investigate the improvement effects of glycyrrhizin (GL) on Helicobacter pylori (HP)-associated gastritis in rats and its mechanism. METHODS HP-associated gastritis rat model was induced by inoculating with 1×109 cfu/mL HP. The model rats were randomly divided into model group, positive control group (HP standard quadruple group), GL low-dose, medium-dose and high-dose groups (5, 20, 50 mg/kg), with 12 rats in each group. Another 12 healthy rats were selected as normal control group. Except the normal control group and model group were given constant volume of normal saline intragastrically, the other groups were given corresponding drugs intragastrically, once a day, for 30 consecutive days. After administration, rats received 13C urea breath test, and delta-over-baseline (DOB) was recorded; the pathological and cellular morphological changes of gastric mucosa in rats were observed, and pathological scoring was performed; the levels of interleukin-8 (IL-8), IL-1β, tumor necrosis factor-α (TNF-α), reactive oxygen species (ROS) and malondialdehyde (MDA) were detected in gastric mucosa of rats; mRNA expressions of high mobility group box-1 protein (HMGB1) and nuclear factor-κ-B (NF-κB), relative expressions of nitric oxide synthases (iNOS) and HMGB1, the phosphorylation level of NF- κBp65 were also detected in rats. RESULTS Compared with normal control group, the DOB value, histopathological score of gastric mucosa, the levels of IL-8, IL-1β, TNF-α, ROS and MDA, relative expressions of HMGB1 and NF- κB mRNA, relative expressions of iNOS and HMGB1 protein and the phosphorylation level of NF-κB p65 were all increased significantly in model group (P<0.05); the epithelial cells of gastric mucosa in rats were incomplete in structure and decreased in the number, with an increase in cell fragments and vacuoles, and significant cell pyknosis. Compared with model group, the changes of the above indexes in GL groups and positive control group were significantly reversed (P<0.05); the changes in the above indicators in the GL high-dose group were more significant than GL low-dose and medium-dose groups (P<0.05); the pathological changes of gastric mucosal cells in rats had all improved. CONCLUSIONS GL may inhibit inflammation and oxidative stress by inhibiting the activation of HMGB1/NF-κB pathway, thus relieving HP-induced gastric mucosal injury.
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Adipose tissue is essential for maintaining systemic metabolic homeostasis through traditional metabolic regulation, endocrine crosstalk, and extracellular vesicle production. Adipose dysfunction is a risk factor for cardiovascular diseases. The heart is a traditional pump organ. However, it has recently been recognized to coordinate interorgan cross-talk by providing peripheral signals known as cardiokines. These molecules include specific peptides, proteins, microRNAs and novel extracellular vesicle-carried cargoes. Current studies have shown that generalized cardiokine-mediated adipose regulation affects systemic metabolism. Cardiokines regulate lipolysis, adipogenesis, energy expenditure, thermogenesis during cold exposure and adipokine production. Moreover, cardiokines participate in pathological processes such as obesity, diabetes and ischemic heart injury. The underlying mechanisms of the cardiac-to-adipose axis mediated by cardiokines will be further discussed to provide potential therapeutic targets for metabolic diseases and support a new perspective on the need to correct adipose dysfunction after ischemic heart injury.
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Objective:To evaluate the role of G-rich RNA sequence binding factor 1 (GRSF1) in cerebral ischemia-reperfusion (I/R) injury in mice and the relationship with ferroptosis.Methods:Twenty-four clean-grade male C57BL/6 mice, aged 8-10 weeks, weighing 20-25 g, were divided into 4 groups ( n=6 each) using a random number table method: sham operation group (Sham group), cerebral I/R group (IR group), cerebral I/R+ GRSF1 overexpression group (IR+ LV-GRSF1 group), and cerebral I/R+ GRSF1 overexpression+ glutathione peroxidase 4 (GPX4) inhibitor group (IR+ LV-GRSF1+ RSL3 group). The model of middle cerebral artery occlusion was developed by thread-occlusion method in anesthetized animals. In IR+ LV-GRSF1 group, GRSF1-overexpressed lentivirus 2 μl was injected into the lateral ventricle at 7 days before the development of the model. GPX4 inhibitor RSL3 5 mg/kg was intraperitoneally injected for 2 consecutive days before the development of the model in IR+ LV-GRSF1+ RSL3 group. After 24 h of reperfusion, the percentage of cerebral infarction volume was determined by TTC assay, the survival neurons in ischemic area were detected by Nissl staining, and brain tissues in ischemic area were obtained for determination of the expression of p16, p21(markers of senescence) and tumor necrosis factor-alpha (TNF-α, senescence-associated secretory phenotype) mRNA (by quantitative real-time polymerase chain reaction), contents of malondialdehyde (MDA), superoxide dismutase(SOD) and glutathione (GSH) (by enzyme-linked immunosorbent assay) and expression of GRSF1, GPX4, Acyl-CoA synthetase long-chain family member 4 (ACSL4) and ferritin (by Western blot). Results:Compared with Sham group, the percentage of cerebral infarction volume was significantly increased, the count of viable neurons was decreased, the expression of p16, p21 and TNF-α mRNA in ischemic brain tissues was up-regulated, SOD and GSH contents were decreased, the MDA content was increased, the expression of GRSF1 and GPX4 was down-regulated, and the expression of ACSL4 and ferritin was up-regulated in IR group ( P<0.05). Compared with IR group, the percentage of cerebral infarction volume was significantly decreased, the count of viable neurons was increased, the expression of p16, p21 and TNF-α mRNA in ischemic brain tissues was down-regulated, SOD and GSH contents were increased, the MDA content was decreased, the expression of GRSF1 and GPX4 was up-regulated, and the expression of ACSL4 and ferritin was down-regulated in IR+ LV-GRSF1 group ( P<0.05). Compared with IR+ LV-GRSF1 group, the percentage of cerebral infarction volume was significantly increased, the count of viable neurons was decreased, the expression of p16, p21 and TNF-α mRNA in ischemic brain tissues was up-regulated, SOD and GSH contents were decreased, the MDA content was increased, the expression of GRSF1 and GPX4 was down-regulated, and the expression of ACSL4 and ferritin was up-regulated in IR+ LV-GRSF1+ RSL3 group ( P<0.05). Conclusions:GRSF1 is involved in the endogenous protective mechanism against cerebral I/R injury by up-regulating GPX4 expression, attenuating oxidative stress, and thus inhibiting ferroptosis in mice.
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OBJECTIVE To study the tocolysis effects of Angelica sinensis polysaccharides on threatened abortion model rats and their impacts on Th1/Th2 balance by regulating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. METHODS Pregnant rats were randomly grouped into the control group, model group, A. sinensis polysaccharide group (200 mg/kg), PI3K/AKT signaling pathway inhibitor LY294002 group (5 mg/kg), and A. sinensis polysaccharide+LY294002 group (200 mg/kg A. sinensis polysaccharide+5 mg/kg LY294002), with 10 rats in each group. Except for the control group, rats in all other groups were given mifepristone (8.3 mg/kg) and misoprostol (100 μg/kg) intragastrically to establish a threatened abortion model, and intragastric or intraperitoneal injection of corresponding drugs. The serum levels of estrogen, progesterone, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin-4 (IL-4) in each group of rats were detected, and the uterine ovarian index and embryonic mortality rate of rats in each group were measured; the morphology of uterine tissue in rats was observed in each group; Th1/Th2 balance in peripheral blood of rats as well as the expression of PI3K/AKT signaling pathway-related proteins in the uterine tissues of rats in each group were detected. RESULTS Compared with the control group, the uterine tissue of rats in the model group showed pathological damage; the serum levels of estrogen, progesterone and IL-4, uterine ovarian index, peripheral blood Th2 cell ratio, and the ratios of phosphorylated PI3K (p-PI3K)/PI3K and phosphorylated AKT (p-AKT)/AKT in uterine tissue were all decreased (P<0.05); the embryo mortality rate, Th1 cell ratio, Th1/Th2 ratio, and serum levels of IFN-γ and TNF-α were increased (P<0.05). Compared with the model group, the pathological damage of uterine tissue in the A. sinensis polysaccharide group was reduced, and the above indexes were all improved significantly (P<0.05); LY294002 could weaken the effect of A. sinensis polysaccharide on model rats (P<0.05). CONCLUSIONS A. sinensis polysaccharides can improve Th1/Th2 imbalance in threatened abortion model rats by activating the PI3K/AKT signaling pathway, thereby inhibiting immune inflammation, and promoting embryo survival.
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Objective To investigate the biological role of methyltransferase-like 14(METTL14)-medi-ated m6A modification in myocardial infarction(MI).Methods A total of 40 mice were randomly divided into 4 groups:Sham+AAV9-NC group(n = 10),Sham+AAV9-METTL14 group(n = 10),MI+AAV9-NC group(n = 10)and MI+AAV9-METTL14 group(n = 10).Mice in each group were injected with AAV9-METTL14 or AAV9-NC through the tail vein one week before MI induction.Cardiac function was measured non-invasively by transthoracic echocardiography,and microvascular injury were measured by immunofluorescence.CMECs were isolated from mouse myocardial tissue,and the cells were treated with oxygen-glucose deprivation(OGD).Results METTL14 was downregulated in MI mouse heart tissue as well as in OGD-treated CMECs.Compared with the Sham+AAV9-NC group,the expression of VE-cadherin was significantly down-regulated(P<0.05),ROS levels increased signifi-cantly(P<0.05)in the MI+AAV9-NC group.MI+AAV9-METTL14 suppressed these changes and enhanced cardiac function in mice.Compared with the NC group,a significant increase in mitochondrial ROS levels was observed in the OGD group(P<0.05).Knockdown of METTL14 in CMECs exacerbated ROS levels(P<0.05),and the addition of USP48 overexpression plasmid reversed these changes(P<0.05).Conclusion METTL14 was lowly expressed in MI and mediates mitochondrial dysfunction in CMECs by increasing the m6A modification level of USP48 in CMECs to reduce its stability.
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Objective To explore the intervention effects of lentinan on sodium arsenite (SA) induced hepatotoxicity in mice. Methods Healthy male C57BL/6 mice were used as experimental subjects and divided into 4 groups, namely control group, SA treatment group, lentinan intervention + SA exposure group, and lentinan intervention control group. The mice were given oral SA (10.0 mg/kg.bw, once every other day) for 14 days, and then the liver tissues and serum samples were collected. Hematoxylin-eosin (HE) was used to evaluate the characteristics of hepatic pathological damage. Enzyme-linked immunosorbent assay (ELISA), Flow Cytometry (FC) and Western-blotting (WB) were used to detect the levels of hepatic function, oxidative stress, CD4+ type 17 helper T cells (Th17), and inflammatory cytokines. Results Compared with the control group, the arsenic exposure group showed obvious hepatic pathological injury and increased levels of serum ALT (8.78±0.76 vs 5.47±0.49) and AST (12.42±1.87 vs 7.14±0.57), FC experiments showed that the Th17 content in liver tissues increased (67.70±4.94 vs 7.36±1.50), and ELISA showed that the antioxidant GSH content decreased (593.40±23.25 vs 730.94±30.81), and the levels of MDA (74.56±7.63 vs 49.90±6.42) and proinflammatory cytokines IL-17A (162.48±10.75 vs 118.53±7.92) and IL-1β (512.50±24.78 vs 462.48±22.15) increased in hepatic tissues (P < 0.05). Compared with the arsenic exposure group, the lentinan showed a significant antagonistic effect after intervention (P < 0.05). Compared to SA exposure group, WB analysis showed that compared with the arsenic exposure group, the expression levels of IL-17A (0.47±0.08 vs 0.89±0.11) and NLRP3 inflammasome (0.80±0.09 vs 1.09±0.16) in the liver tissues of the lentinan intervention group were significantly decreased (P < 0.05). Conclusion Lentinan alleviates SA-induced hepatic injury in mice, which may be mediated through the inhibition of Th17-IL-17A inflammatory signaling.
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Previous studies focused on the unique regulatory mechanisms of different cell death pathways. However, recent studies highlight crosstalk and co-ordination between these pathways and initiate a new cell death process called PANoptosis (pyroptosis, apoptosis, necroptosis). PANoptosis is an inflammatory programmed cell death pathway regulated by the PANoptosome complex with critical features of pyroptosis, and/or necroptosis but cannot be characterized by any of the death modes of pyroptosis, apoptosis or necroptosis alone. By activating the PANoptosis pathway, some triggers like bacterial, viral, and fungal infections can cause death of the host. This review explains the PANoptosis-related routes, regulators and their potential effects on blinding eye diseases.
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Atherosclerosis is a chronic inflammatory disease of vascular walls with a complex etiology. In recent years, the incidence of atherosclerosis continues to increase with obesity and diabetes as major risk factors. As an important metabolic organ in the body, adipose tissue also has a powerful endocrine function. In the case of obesity and diabetes, various cytokines and exosomes derived from adipose tissue mediate organ-organ/cell-cell crosstalk, and are involved in the occurrence and development of various diseases. As an important intercellular communicator, exosomes regulate the pathological process of various cardiovascular diseases and are closely related to atherosclerosis. In this paper, we reviewed the mechanism of adipose-derived exosomes in atherosclerosis with focus on endothelial dysfunction, inflammatory response, lipid metabolism disorder and insulin resistance, hoping to provide reference for the research, diagnosis and treatment of atherosclerosis.
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Humans , Exosomes/metabolism , Atherosclerosis , Obesity/complications , Adipose Tissue/metabolism , Insulin ResistanceABSTRACT
OBJECTIVE@#To assess the safety and efficacy of Neuroform Atlas stent used in treatment of unruptured wide-neck intracranial aneurysms.@*METHODS@#Clinical data of 62 patients with unruptured wide-neck intracranial aneurysms undergoing Neuroform Atlas stent-assisted coiling from August 2020 to September 2021 were retrospectively analyzed. There were 64 aneurysms in those 62 patients. Among them, 25 aneurysms were located at the bifurcation of M1 segment on middle cerebral artery, 16 at the anterior communicating artery, 10 at the C7 segment of internal carotid artery, 5 at the C6 segment of internal carotid artery, 4 at the apex of basilar artery, 3 at the A3 segment of anterior cerebral artery, and 1 at the M2 segment of middle cerebral artery. All the patients underwent Neuroform Atlas stent-assisted coiling, including 49 patients with single stent assisted coiling and 15 patients with dual stents assisted coiling (14"Y"style and 1"X"style). After the procedure, the immediate DSA was performed to evaluate the status of aneurysm occlusion and the parent artery patency. The clinical follow-up was performed 3 months after the operation and evaluated based on the modified Rankin Scale(mRS).DSA image was reviewed at 6 months after operation and Raymond grading scale was used to assess the status of aneurysm occlusion and the parent artery patency.@*RESULTS@#A total of 62 patients with 64 aneurysms were all achieved technical success(100%).The immediate post-procedural Raymond scale was assessed, including Raymond Ⅰ in 57 aneurysms(89.1%, 57/64), Raymond Ⅱ in 6 aneurysms(9.3%, 6/64) and Raymond Ⅲ in 1 aneurysm(1.6%, 1/64). The peri-procedural complications rate was 4.8%(3/62), 2 patients developed intraoperative thrombosis and 1 patient suffered from local subarachnoid hemorrhage. Among them, 55 patients obtained 3 months clinical follow-up after operation and all the patients had good outcomes (mRS≤2), 50 patients with 52 aneurysms were followed up with DSA 6 months after operation, including Raymond Ⅰ in 45 aneurysms(86.5%, 45/52), Raymond Ⅱ in 4 aneurysms(7.7%, 4/52) and Raymond Ⅲ in 3 aneurysms(5.8%, 3/52).@*CONCLUSION@#Neuroform Atlas stent for the treatment of unruptured wide-neck intracranial aneurysms has high safety and good efficacy, and has its advantages over other traditional stents.
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Humans , Intracranial Aneurysm/etiology , Retrospective Studies , Treatment Outcome , Embolization, Therapeutic/methods , Stents/adverse effects , Cerebral AngiographyABSTRACT
OBJECTIVE@#To investigate the role of multiple serological methods in the identification of complex antibodies.@*METHODS@#The blood group antigens were detected by saline and microcolumn agglutination methods. The saline method was used to screen and identify IgM-type antibodies in the patient's serum, while the polybrene, anti-globulin, microcolumn agglutination, enzymic and absorption-elution methods were used to screen and identify IgG-type antibodies.@*RESULTS@#The patient was B/CCDee/Jk(a-b+)/Fy(a-b+) blood type. The serum reacted with panel cells, and the reaction presented anti-E pattern in the saline medium. It was fully positive in the microcolumn agglutination card, except 2 negative ones after using papain to treat the panel cells. Referring to the pattern table, it was concluded that there existed anti-c, anti-E, and anti-Jka antibodies, and one antibody corresponding to an antigen that was easily destroyed by papain. The red blood cells with specific phenotype were selected for absorption-elution to identify IgG-type anti-c, anti-E, anti-Jka and anti-Fya antibodies.@*CONCLUSION@#It is confirmed that IgM-type anti-E, and IgG-type anti-c, anti-E, anti-Jka and anti-Fya antibodies exist in the patient's serum by multiple serological methods.
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Humans , Papain , Blood Group Antigens , Erythrocytes , Immunoglobulin G , Immunoglobulin MABSTRACT
HMGB1's role in tumors is complex and diverse,and it exerts its biological function by combining with different receptors.One of the receptors is called RAGE,which is localized to the cell membrane and binds to HMGB1 released outside the cell.The HMGB1/RAGE axis promotes tumor development,moreover,tumor development and its drug resistance are closely related to inflammation.This article mainly reviews the molecular mechanism of HMGB1/RAGE axis in pro-inflammatory and protumor effects in pancreatic,colorectal and liver cancers.We also summarize the research progress of papaverine and its derivatives for the treatment of HMGB1/RAGE axis in tumor inflammation,with aims of providing new ideas for exploring the molecular mechanism of action in tumor inflammation,and providing a new theoretical basis for the research of HMGB1/RAGE axis therapeutics.
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OBJECTIVE To investigate the impacts of isorhynchophylline (IRN) on airway inflammation in asthmatic mice by regulating the monocyte chemotactic protein-1 (MCP-1)/CC chemokine receptor 2 (CCR2) signaling pathway. METHODS The asthmatic mice model was established by injecting and inhaling ovalbumin. The successfully modeled mice were randomly grouped into asthma group, IRN low-dose group (IRN-L, intragastric administration of 10 mg/kg IRN), IRN high-dose group (IRN-H, intragastric administration of 20 mg/kg IRN), IRN-H+CCL2 group [intragastric administration of 20 mg/kg IRN+intraperitoneal injection of 7.5 ng CC chemokine ligand 2 (CCL2)] and positive control group (intraperitoneal injection of 2 mg/kg dexamethasone). The mice injected and inhaled with sterile phosphate-buffered solution were included in the blank control group, with 10 mice in each group. The mice in administration groups were given relevant medicine once a day, for consecutive 2 weeks. The levels of airway hyperreactivity indexes such as enhanced (Penh) value, tumor necrosis factor-α (TNF-α),interleukin-13 (IL-13) and IL-4 in serum, the number of eosinophil (EOS), lymphocyte (LYM) and neutrophils (NEU) in alveolar lavage fluid and the protein expressions of MCP-1 and CCR2 in lung tissue were observed in each group; the pulmonary histopathological changes were observed, and inflammatory cell infiltration score was evaluated. RESULTS Compared with the blank control group, the infiltration of inflammatory cells in the lung tissue of mice was more significant in the asthma group, and there was swelling and shedding of cells; inflammatory infiltration score, Penh value, the levels of IL-4, IL-13 and TNF-α, the number of EOS, NEU and LYM, the protein expressions of MCP-1 and CCR2 were increased significantly (P<0.05). Compared with the asthma group, the pathological injuries of the IRN-L group, IRN-H group and positive control group were improved, and the above quantitative indexes were decreased significantly (P<0.05). Compared with the IRN-L group, the above quantitative indexes of the IRN-H group and positive control group were decreased significantly (P<0.05). There was no statistical significance in the above quantitative indexes between the IRN-H group and the positive control group (P>0.05). Compared with the IRN-H group, the above quantitative indexes of the IRN-H+CCL2 group were increased significantly (P<0.05). CCL2 reversed the protective effect of high-dose IRN on asthmatic mice. CONCLUSIONS IRN may reduce the release of airway inflammatory factors in asthmatic mice by inhibiting the activation of the MCP-1/CCR2 signaling pathway, so as to achieve the purpose of improving asthma.
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Ischemic preconditioning (IPC) is a potential intervention known to protect the heart against ischemia/reperfusion injury, but its role in the no-reflow phenomenon that follows reperfusion is unclear. Dihydrotanshinone I (DT) is a natural compound and this study illustrates its role in cardiac ischemic injury from the aspect of IPC. Pretreatment with DT induced modest ROS production and protected cardiomyocytes against oxygen and glucose deprivation (OGD), but the protection was prevented by a ROS scavenger. In addition, DT administration protected the heart against isoprenaline challenge. Mechanistically, PKM2 reacted to transient ROS via oxidization at Cys423/Cys424, leading to glutathionylation and nuclear translocation in dimer form. In the nucleus, PKM2 served as a co-factor to promote HIF-1α-dependent gene induction, contributing to adaptive responses. In mice subjected to permanent coronary ligation, cardiac-specific knockdown of Pkm2 blocked DT-mediated preconditioning protection, which was rescued by overexpression of wild-type Pkm2, rather than Cys423/424-mutated Pkm2. In conclusion, PKM2 is sensitive to oxidation, and subsequent glutathionylation promotes its nuclear translocation. Although IPC has been viewed as a protective means against reperfusion injury, our study reveals its potential role in protection of the heart from no-reflow ischemia.
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AIM: To explore the expression and significance of forkhead box class O3(FOXO3)and interleukin-2(IL-2)in conjunctival epithelial cells and tears of patients with dry eye(DE).METHODS:A perspective study. A total of 106 DE patients who accepted from March 2019 to March 2021 were prospectively gathered, and 85 healthy subjects in the same period were selected as the control group. The level of FOXO3 in the conjunctival epithelial cells and tear fluid was measured by real-time fluorescent quantitative PCR(qRT-PCR)method; The level of IL-2 in the sample was measured by enzyme-linked immunosorbent(ELISA)method; The changes in clinical indicators of the ocular surface such as break-up time(BUT), Schirmer Ⅰtest(SⅠt), cornea fluorescein staining(CFS)in DE patients before and after treatment were analyzed; The correlation between the levels of FOXO3 and IL-2 in the conjunctival epithelial cells and tears of DE patients and the relationship between the two and clinical indicators were analyzed by Pearson correlation analysis.RESULTS:Compared with the control group, the level of FOXO3 in conjunctival epithelial cells and tear fluid in the DE group was obviously reduced, and the level of IL-2 was obviously increased(all P<0.01). Compared with before treatment, the level of FOXO3 in conjunctival epithelial cells and tear fluid of DE patients was obviously up-regulated, and the level of IL-2 was obviously down-regulated(all P<0.05). Pearson correlation analysis showed that the levels of FOXO3 and IL-2 in conjunctival epithelial cells and tear fluid were obviously inversely correlated(r=-0.531, -0.469, all P<0.01). After treatment, BUT and SⅠt indexes of DE patients increased compared with before treatment, while CFS decreased(all P<0.01). The level of FOXO3 in conjunctival epithelial cells of DE patients was obviously directly correlated with BUT and SⅠt(r=0.431, 0.457, all P<0.01), and it was obviously inversely correlated with CFS(r=-0.469, P<0.01), and the level of IL-2 was obviously inversely correlated with BUT and SⅠt(r=-0.416, -0.447, all P<0.01), and it was obviously directly correlated with CFS(r=0.424, P<0.01); tear FOXO3 was positively correlated with BUT and SⅠt(r=0.421, 0.443, all P<0.01), and it was negatively correlated with CFS(r=-0.474, P<0.01), and IL-2 was negatively correlated with BUT and SⅠt(r=-0.408, -0.429, all P<0.01), and it was positively correlated with CFS(r=0.419, P<0.01).CONCLUSION: the level of FOXO3 in conjunctival epithelial cells and tears of DE patients is decreased, and the level of IL-2 is increased. The two of which are closely related to the ocular surface indicators of patients. They are expected to become laboratory auxiliary indicators for clinical monitoring and prognostic evaluation of DE.
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Atractylodis Rhizoma is a kind of commonly used clinical Chinese medicine (TCM), which was first recorded in Shennong Bencaojing (《神农本草经》). At that time, it was called "Zhu", which is the general name of Atractylodis Rhizoma and Atractylodis Macrocephalae Rhizoma. After Song dynasty, Atractylodis Rhizoma and Atractylodis Macrocephalae Rhizoma were separated. Atractylodis Rhizoma can be divided into Atractylodes lancea and A. chinensis. In history, A. lancea as authentic, that its quality is better than A. chinensis. However, the quality of Atractylodis Rhizoma was evaluated by the index component atractylodin in the 2020 edition of Chinese Pharmacopoeia. The general results showed that the content of atractylodin in A. lancea was low, even failed to meet the specified standard, and its content in A. chinensis was significantly higher than that in A. lancea. The results were inconsistent with the records of ancient books and documents, and the quality theory of "genuine medicine is the best". It could not reflect the quality advantage of genuine Atractylodis Rhizoma, and may even affect the clinical application and development momentum of genuine medicine. In short, the quality standard of TCM should not only conform to the historical experience, but also have the connotation of modern science and technology, which can stand the test of practice. Based on this, the author intends to sort out relevant laws and regulations, sort out the literature related to the authenticity, composition and efficacy of Atractylodis Rhizoma, and analyze the rationality of the current standard of Atractylodis Rhizoma by integrating the relevant records of historical classics and modern research results, so as to provide a basis for the improvement of the quality standard of Atractylodis Rhizoma.
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Objective:To evaluate the relationship between the second messenger cyclic GMP-AMP (cGAS)-cyclic GMP-AMP receptor stimulator of interferon genes (STING) signaling pathway and ferritinophagy in the early stage of cerebral ischemia-reperfusion (I/R) in mice.Methods:Twenty-four clean-grade healthy male C57BL/6 mice, aged 6-8 weeks, weighing 21-25 g, were divided into 4 groups ( n=6 each) using a random number table method: sham group, cerebral I/R injury group (CIRI group), cerebral I/R injury + cGAS inhibitor group (CIRI + RU group), and cerebral I/R injury + cGAS inhibitor + overexpressed nuclear receptor coactivator 4 (NCOA4) group (MCAO + RU + LV-NCOA4 group). The model of cerebral I/R injury was developed using the middle cerebral artery occlusion (MCAO) in anesthetized animals.In CIRI+ RU group, cGAS inhibitor 5 mg/kg was intraperitoneally injected at 10 min before reperfusion.In CIRI+ RU+ LV-NCOA4 group, NCOA4-overexpressing lentivirus (1×10 9 TU/ml) 2 μl was injected into the ventricle at 7 days before MCAO, and the other operations were the same as those previously described in CIRI+ RU group.After 6 h of reperfusion, the neurological function deficits were assessed and scored, then the mice were sacrificed, and brains were removed for determination of the cerebral infarct size (by TTC method), MDA content (by TBA method), activity of SOD (by WST-1 method), and expression of cGAS, STING, NCOA4, ferritin, and microtubule-associated protein 1 light chain 3B (LC3B) (by Western blot). Results:Compared with Sham group, the neurological function deficit score and cerebral infarct size were significantly increased, SOD activity was decreased, MDA content was increased, the expression of cGAS, STING, NCOA4 and LC3B was up-regulated, and the expression of ferritin was down-regulated in CIRI group ( P<0.05). Compared with CIRI group, the neurological function deficit score and cerebral infarct size were significantly decreased, SOD activity was increased, MDA content was decreased, the expression of cGAS, STING, NCOA4 and LC3B was down-regulated, and the expression of ferritin was up-regulated in CIRI+ RU group ( P<0.05). Compared with CIRI+ RU group, the neurological function deficit score and cerebral infarct size were significantly increased, SOD activity was decreased, MDA content was increased, the expression of cGAS, STING, NCOA4 and LC3B was up-regulated, and the expression of ferritin was down-regulated in CIRI group ( P<0.05), and no significant change was found in the expression of cGAS and STING in CIRI+ RU+ LV-NCOA4 group ( P>0.05). Conclusions:The cGAS-STING signaling pathway can promote the over-activation of ferritinophagy, enhance oxidative stress, and thus induce early CIRI in mice.
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This study investigated whether the mitochondrial-targeted peptide SS-31 can protect against cigarette smoke- (CS-) induced airway inflammation and oxidative stress in vitro and in vivo. Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure. Pathologic changes and oxidative stress in lung tissue, inflammatory cell counts, and proinflammatory cytokine levels in bronchoalveolar lavage fluid (BALF) were examined. The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues. SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF. SS-31 also attenuated CS-induced oxidative stress by decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) activities and increasing that of superoxide dismutase (SOD). It also reversed CS-induced changes in the expression of mitochondrial fission protein (MFF) and optic atrophy (OPA) 1 and reduced the amount of cytochrome c released into the cytosol. Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression. RNA sequencing and western blot analysis showed that SS-31 inhibited CS-induced activation of the mitogen-activated protein kinase (MAPK) signaling pathway in vitro and in vivo. Thus, SS-31 alleviates CS-induced airway inflammation and oxidative stress via modulation of mitochondrial function and regulation of MAPK signaling and thus has therapeutic potential for the treatment of airway disorders caused by smoking.
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Antioxidants/therapeutic use , Inflammation Mediators/therapeutic use , Inflammation/drug therapy , Lung Diseases/drug therapy , Lung Diseases/etiology , Lung/pathology , Oligopeptides/therapeutic use , Smoke/adverse effects , Animals , Antioxidants/pharmacology , Humans , Lung Diseases/pathology , Male , Mice , Oligopeptides/pharmacology , Oxidative StressABSTRACT
Rescuing cells from stress damage emerges a potential therapeutic strategy to combat myocardial infarction. Protocatechuic aldehyde (PCA) is a major phenolic acid in Chinese herb Danshen (
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OBJECTIVE: To analyze the abnormal results and their causes of personal dose monitoring on medical radiation workers.METHODS: The medical radiation workers monitored from 2016 to 2019 in the personal dose monitoring room of Guangdong Province Hospital for Occupational Disease Prevention and Treatment were selected as the study subjects using convenient sampling method. The abnormal results and their causes of the medical radiation workers with personal dose equivalent ≥1.25 mSv(investigation level) in a single period were analyzed. RESULTS: The rate of abnormal results of personal dose monitoring was 0.26%(263/102 284). The false result rate was 0.19%(194/102 284), and that of the true result rate was 0.07%(69/102 284). A total of 73.38%(193/263) of medical radiation workers had abnormal results with an personal dose equivalent less than 5.00 mSv. Among different occupational groups, the abnormal results and false results in personal dose monitoring in interventional radiology group were the highest(all P<0.01). The abnormal result rate and false result rate were higher in the Pearl River Delta area than that in the non-Pearl River Delta area(0.27% vs 0.17%, 0.20% vs 0.12%, all P<0.05). The rate of false result of personal dose monitoring in the tertiary hospitals was lower than that in the non-tertiary hospitals(0.18% vs 0.30%, P<0.05). The main reason for the true results of personal dose monitoring was the increase of workload(43.48%), and the main reason for the false results was that the dosimeter was left in the workplace(57.73%). CONCLUSION: The rate of abnormal results of personal dose monitoring in the medical radiation workers is high. Radiological protection should be strengthened with emphasis on medical radiation workers in interventional radiology, Pearl River Delta area hospitals and non-tertiary hospitals.
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Objective:To provide scientific evidence for infection prevention and control by analyzing the risk factors of surgical site infection, which can move forward the gateway of infection prevention and control.Methods:The surgery-related information of patients admitted to the Department of General Surgery and Department of Orthopedics, People's Hospital of Guangnan Hospital of Yunnan province from November 2016 to August 2019 was retrospectively analyzed. According to whether postoperative surgical site infection occurred, the patients were divided into an infection group and a non-infection group. Logistic regression model was used to analyze the risk factors of surgical site infection.Results:A total of 9 346 patients, consisting of 117 patients in the infection group and 9 229 patients in the non-infection group, were included for final analysis. In the infection group, the incidence of surgical site infection was 1.25%. Multivariate analysis showed that hypoproteinemia ( OR = 2.585), unclean incision ( OR = 3.243 and 5.125), and operation duration more than 3 hours ( OR = 2.315), blood transfusion ( OR = 2.239), drainage tube placement ( OR = 2.133) and indwelling catheter placement ( OR = 1.973) were the independent risk factors for surgical site infection, while prophylactic use of antibiotics was a protective factor ( OR = 0.383). Conclusion:Individual factors, operation-related factors, and treatment-related factors are closely related to the occurrence of surgical site infection. Much attention should be paid to the clinical issues like preoperative hypoproteinemia, perioperative prophylactic use of antibiotics and postoperative drainage tube and indwelling catheter placement.