Obesity exacerbates pathological injury in chronic kidney disease and ultimately leads to end-stage renal fibrosis. Extensive studies have demonstrated that scutellarin (SCU), the major active component of the traditional Yunnan medicinal herb Erigeron breviscapus, effectively attenuates tissue fibrosis. However, the molecular mechanisms underlying the protective effects of SCU against obesity-induced renal fibrosis remain unclear. In this study, we first established a high-fat diet (HFD)-induced rat model of renal fibrosis. We assessed renal function, renal morphology, fibrosis-related protein expression, and apoptotic phenotypes. These analyses demonstrated that SCU effectively alleviated renal fibrosis in HFD-fed rats. Consistently, these findings were further validated in a palmitate (PA)-induced HK-2 cell model of renal fibrosis. Subsequently, bulk RNA sequencing identified integrin α9 (ITGA9) as a potential target of SCU. Molecular docking (mean affinity -6.92 ± 0.17 kcal/mol; predicted Ki ≈ 8.46 μM) and surface plasmon resonance (SPR; KD = 5.73 × 10⁻⁶ M) consistently supported a direct interaction between SCU and ITGA9, although the precise binding site was not defined and additional molecular targets of SCU cannot be excluded. ITGA9 was further silenced or overexpressed in HK-2 cells to validate its functional role in renal fibrosis. Subsequent analyses identified the FAK/PI3K/AKT signaling pathway as a key downstream cascade of ITGA9. This pathway was further verified in renal tissues from HFD-fed rats and in HK-2 cells. Our study indicates that SCU alleviates obesity-associated renal injury and tubular epithelial fibrotic responses at least partly through ITGA9, with consequent suppression of FAK/PI3K/AKT signaling in this lipid-overload setting. ITGA9 dependence is most directly supported in PA-treated HK-2 cells, whereas the in vivo data support association and pathway consistency.

Type 1 diabetes mellitus (T1DM) and cognitive impairment (CI) are diseases impacting human health. Mild cognitive impairment (MCI), a critical stage of cognitive impairment, is strongly associated with T1DM relating to energy metabolism. Mitochondria, the intracellular energy factories, implicated in diabetic MCI. Therefore, identifying a mitochondrial related biomarker and investigate its role in diabetic MCI are profound. In this study, based on human blood gene datasets obtained from public database, 4 key mitochondrial factors ACADVL, HSPE1, LYPLAL1 and UQCRH were identified by performing differential analysis, functional enrichment analysis and machine learning. To validate these four factors, T1DM mice exhibiting CI and hippocampal damage were observed, UQCRH (a component of mitochondrial complex III) expression reduction was the most obvious amount these four factors in hippocampus, when it was validated in another related dataset. In order to further confirming the role of UQCRH in diabetic MCI, AAV expressing UQCRH intracerebral injection was performed, cognitive impairment of T1DM mice were attenuated post AAV intracerebral injection. Taken together, this study indicated hippocampal mitochondrial dysfunction was involved in diabetic MCI. UQCRH, could be recognized as a biomarker for diabetic MCI, elevating UQCRH expression further improving mitochondrial function served as a potential treatment for diabetic MCI.

Diabetic cardiomyopathy (DCM) is an important cause of death in patients with diabetes. DCM can be simulated by cardiomyocyte injury induced by high glucose (HG) in vitro. Scutellarin (Scu) is a flavonoid extracted from Erigeron breviscapus. The H9c2 cell line was used as an in vitro model in the present study to investigate the mechanism by which Scu reduces HG-induced cardiomyocyte injury. Moreover, the present study aimed to provide scientific evidence on the mechanism by which Scu prevents DCM. The following groups were used: Control, model, Scu (50/100/200/400 µM) and curcumin. Following H9c2 cell adherence, the control and model groups were treated with normal medium; the Scu group cells were treated with different concentrations of Scu, whereas the curcumin group cells were treated with 4 µM curcumin for 4 h. Subsequently, the normal group was cultured in normal medium, and the other groups were treated with medium containing 100 mM HG for 48 h. The results indicated that Scu improved the morphology of H9c2 cells treated by HG, enhanced cell proliferative activity, reduced the production of reactive oxygen species and the induction of apoptosis. Moreover, Scu promoted the expression of Bcl-2 and inhibited the expression levels of caspase-3, cleaved caspase-3, caspase-9, cleaved caspase-9, caspase-12, Bax, NADPH oxidase (Nox)2 and Nox4. The findings indicated that Scu could inhibit oxidative stress and reduce the induction of apoptosis in cardiomyocytes, thereby alleviating HG-induced myocardial injury.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a metabolic disease. Scutellarin (Scu) is one of the active components extracted from Erigeron breviscapus (Vaniot) Hand.-Mazz., which has been shown to fight multiple diseases. However, there is not enough evidence to support the effectiveness of Scu in treating MASLD. We aimed to investigate whether Scu could be a potential drug for MASLD. The rat model of MASLD was established after a high-fat and high-sugar (HFHS) diet for 16 weeks. After the model had been successfully built, 100 mg/kg/d Scu was given for 8 weeks. The biochemical indexes of serum were determined by an automatic biochemical analyzer. The process involved staining liver tissues by oil red "O" and hematoxylin and eosin (HE) staining, followed by the extraction of total RNA from the liver. Then, high-throughput sequencing was used to screen the changes in the transcriptome. Verification of the associated key genes was achieved through bioinformatics, Western blot, RT-PCR, and immunohistochemical analyses. The results demonstrated that Scu could decrease the ratio of liver weight to body weight, as well as the levels of ALT, AST, ALP, TG, and TC in SD rats induced by HFHS diets, thereby improving liver function and lipid accumulation in rats. Furthermore, Scu was capable of reversing pathological changes in SD rats. The transcriptomic analysis corroborated these findings and further identified Pdk4 as a crucial gene mediating the beneficial effects of Scu on MASLD in rats. This was also supported by RT-PCR, Western blot, and immunohistochemical analyses. This study is the first to identify Pdk4 as a key gene for Scu treatment of MASLD through transcriptomes and confirms that Scu is a potentially effective drug for MASLD.

Renal fibrosis is characterized by the formation of scar tissue in the kidney parenchyma. Obesity, with its rising global incidence, has become a significant cause of renal fibrosis. This study investigates the effect of Scutellarin (SCU) on obesity-induced renal fibrosis. Rats were fed a high-fat and high-sugar diet (HFSD) for 40 weeks. SCU was administered orally at doses of 25, 50, and 100 mg/kg/day during the last 8 weeks. Metabolic function was assessed by measuring serum triglycerides (TG), total cholesterol (TC), and glucose levels. Renal function was evaluated by analyzing serum uric acid (UA), creatinine (CRE), and blood urea nitrogen (BUN). RNA-seq was used to evaluate transcriptome changes in the kidney. Histopathological changes were examined using HE and Masson staining. Protein expressions and localization of FOS, JUN, FN, and TGF-β1 were analyzed by western blot, immunohistochemistry, and immunofluorescence. HFSD-fed rats exhibited significant increases in body weight, serum TG, TC, and glucose levels, alongside elevated UA, CRE, and BUN levels, indicating metabolic and renal dysfunction. SCU treatment significantly improved these metabolic and renal parameters across all doses. Biochemical analyses and RNA-seq results confirmed the absence of dose-dependency in the effects of SCU. Histopathological analysis showed a reduction in glomerular hypertrophy and collagen deposition in the SCU-treated groups. RNA-seq data indicated a downregulation of Activator Protein 1 (AP-1), composed of FOS and JUN, at the transcriptional level. Western blot analysis confirmed that SCU treatment reduced both the expression and phosphorylation levels of FOS and JUN. Additionally, SCU downregulated the expression of fibrosis-related proteins TGF-β1 and FN, contributing to a reduction in renal fibrosis. SCU alleviates obesity-induced renal fibrosis through the downregulation of AP-1 activity and the expression level of fibrosis-related proteins TGF-β1 and FN.

The immune system is involved in the development and progression of several diseases. Type 1 diabetes mellitus (T1DM), an autoimmune disorder, influences the progression of several other conditions; however, the link between T1DM and mild cognitive impairment (MCI) remains unclear. This study investigated the underlying immune response mechanisms that contribute to the development and progression of T1DM and MCI. Microarray datasets for MCI (GSE63060) and T1DM (GSE30208) were retrieved from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified using the limma package. To explore the functional implications of these DEGs, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were conducted using ClusterProfiler. Protein-protein interaction networks for the DEGs were constructed using the STRING database and visualized using Cytoscape. The Molecular Complex Detection algorithm was used to analyze DEGs. Immune cell infiltration in patients with T1DM and MCI was analyzed using the xCell method. Gene set enrichment analysis was used to gain in-depth insights into the functional characteristics of T1DM and MCI. Immune-related genes were obtained from the GeneCards and ImmPort databases. Machine learning algorithms were used to identify potential hub genes associated with immunity for T1DM and MCI diagnosis, and the diagnostic value was assessed using the receiver operating characteristic curve. The identified genes were validated using quantitative polymerase chain reaction. In the T1DM and MCI datasets, 610 DEGs showed consistent trends, of which 232 and 378 were upregulated and downregulated, respectively. Immune response analysis revealed significant changes in the immune cells associated with MCI and T1DM. Using immune-related genes, DEGs, and machine learning techniques, we identified CD3D in the MCI and T1DM groups. We observed a gradual decline in the cognitive function of mice with T1DM as the disease progressed. CD3D expression increased with increasing disease severity; CD3D primarily affected CD4+ T cells. This study revealed a complex interaction between T1DM and MCI, providing novel insights into the intricate relationship between immune dysregulation and cognitive impairment and expanding our understanding of these two interconnected disorders. These findings will facilitate the development of therapeutic interventions and identification of potential therapeutic targets.

Background: Cognitive impairment is a common manifestation in patients with T2DM mellitus (T2DM). Ginsenoside Rg1 (GRg1) is the main active substance extracted from ginseng or Panax notoginseng. Methods: T2DM was induced by feeding rats with a high-sugar and high-fat diet combined with a low-dose intraperitoneal injection of streptozotocin (STZ, 35 mg/kg) on an empty stomach. Subsequently, different concentrations of GRg1 (25, 50, 100 mg/kg/d) were used to intervene for 8 weeks and explore its therapeutic effects and potential mechanisms on cognitive impairment in T2DM rats. Results: Our data suggested that administration of GRg1 improved insulin resistance, specifically manifesting in a reduction of insulin resistance index by approximately 57.1 % with high doses of GRg1 (100 mg/kg/d). Besides, it has been observed to lower cholesterol, triglycerides, and low-density lipoprotein by approximately 20-50 % in T2DM rats. In addition, GRg1 treatment dramatically improved the spatial memory and learning ability in T2DM rats. Furthermore, administration of GRg1 to the T2DM rats dose-dependently up-regulated ERKs phosphorylation and blunted phosphorylation of JNKs and p38. Furthermore, GRg1 treatment also dose-dependently increased the expression of Bcl-2 but inhibited the expression of Bax and Caspase 3 expression in T2DM rats brain cortex and hippocampus neurons. Conclusion: GRg1 effectively improves mild cognitive impairment in T2DM rats by inhibiting oxidative stress and reducing the apoptosis of neurons in the cerebral cortex and hippocampus.

目的 研究在高脂高糖饮食诱导建立的肥胖大鼠慢性肝损伤肝脏纤维化模型中,灯盏乙素(SCU)对其发病机制的影响,探讨SCU能否通过促进MMP2、MMP9,抑制TIMP-1的表达改善肝脏纤维化程度.方法 采用高脂高糖饮食诱导慢性肝损伤肝脏纤维化模型,SCU和姜黄素(CUR)灌胃治疗8周后,HE染色观察肝组织病理变化;Masson染色观察胶原纤维在肝脏中的沉积;Western blot和免疫组织化学染色观察肝脏组织TIMP-1、MMP2、MMP9的表达.结果 在肝脏组织中,模型组大鼠肝细胞形态不规则细胞水肿,并有大量脂肪空泡出现,汇管区有蓝色胶原纤维沉积,不同剂量的SCU和CUR干预后,脂肪空泡减少,肝细胞肿胀情况减少,纤维化程度得到改善.在大鼠肝细胞中,模型组MMP2、MMP9蛋白表达下调(P<0.01),不同剂量SCU和CUR干预后MMP2、MMP9蛋白表达上调(P<0.01);模型组TIMP-1蛋白表达上调(P<0.01),不同剂量SCU和CUR治疗后TIMP-1蛋白表达下调(P<0.01),没有很明显的剂量依赖性.结论 SCU可能通过促进MMP2、MMP9,抑制TIMP-1蛋白的表达,减少ECM的积累改善肥胖引起的肝脏纤维化.

为筛选出用于预防高糖诱导的H9 c2细胞损伤的最适姜黄素浓度,检测不同浓度姜黄素处理下H9 c2细胞的部分指标的表达,并观察细胞形态变化.结果显示,与模型组相比,姜黄素浓度为4×10-6,8×10-6和20×10-6 mol/L时细胞增殖活力上升;姜黄素各组的Caspase 3和Cleaved-Caspase 3的蛋白表达均显著下调;姜黄素4×10-6 mol/L时,H9c2细胞形态和数量恢复,且分布均匀,排列紧密,与正常组细胞无较大差异.最终选择4×10-6 mol/L时的姜黄素作为预防高糖诱导的H9c2细胞损伤的最适浓度.

ObjectObesity is an increase in body weight beyond the limitation of skeletal and physical requirement, as the result of an excessive accumulation of fat in the body. Obesity could increase the risk of myocardial fibrosis. (-)-Epigallocatechin-3-gallate (EGCG) is the most abundant substance in green tea and has been reported to have multiple pharmacological activities. However, there is not enough evidence to show that EGCG has a therapeutic effect on obesity-induced myocardial fibrosis. This study aims to investigate whether EGCG is a potential drug for obesity-induced myocardial fibrosis.MethodsObesity-induced myocardial fibrosis rat model was established by HFD feeding for 36 weeks. EGCG was intragastrically administered at 160 mg/kg/d for the last 4 weeks. The pathological changes of myocardial fibrosis were evaluated by tissue pathological staining and collagen quantification. Furthermore, total RNA was extracted from the heart for RNA-seq to identify the changes in the transcript profile, and the relevant hub genes were verified by quantitative real-time PCR and western blot.ResultsEGCG significantly relieved HFD diet-induced obesity and alleviated the pathology of myocardial fibrosis. Biochemical analysis showed that EGCG could relieve the burden of lipid metabolism and injury to the myocardium and transcript profile analysis showed that EGCG could alleviate obesity-induced myocardial fibrosis by increasing the level of Scn5a in the heart. Furthermore, quantitative real-time PCR and western blot analysis for SCN5A also confirmed this finding.ConclusionTaken together, these results suggest that EGCG could protect against the obesity-induced myocardial fibrosis. EGCG plays an anti-myocardial fibrosis role by regulating the expression of SCN5A in the heart.

目的 研究表没食子儿茶素没食子酸酯(epigallocatechin gallate,EGCG)对高脂高糖饮食诱导的肥胖大鼠心肌纤维化影响,探讨EGCG能否通过TGF-β 1/Smads信号通路减轻心肌纤维化的程度.方法 采用长期高脂高糖饮食形成肥胖大鼠模型,给予EGCG每天灌胃,治疗4周后,称取各组大鼠体重,Masson染色检测心肌纤维化的程度.生化检测血清中空腹血糖(FBG)、甘油三酯(TG)、总胆固醇(TC)、丙二醛(MDA)和谷胱甘肽(GSH)的含量.Western blotting检测各组大鼠心脏组织中相关蛋白(Collagen Ⅰ、Collagen Ⅲ、TGF-β 1、Smad2/3,p-Smad2/3、Smad7)的表达水平.结果 与正常组比较,模型组大鼠体重增加,给予EGCG治疗后减轻.与正常组比较,模型组大鼠心肌纤维化程度严重,给予EGCG治疗后减轻.与正常组比较,模型组大鼠FBG、TC、TG、MDA高于正常组,给予EGCG治疗后下降.与正常组比较,模型组大鼠GSH活性低于正常组,给予EGCG治疗后升高.与正常组比较,模型组大鼠Collagen Ⅰ、Collagen Ⅲ、TGF-β 1、Smad2/3、p-Smad2/3蛋白表达升高,给予EGCG治疗后下降.与正常组比较,模型组大鼠Smad7蛋白表达低于正常组,给予EGCG治疗后升高.结论 EGCG能够改善肥胖大鼠血糖和脂质代谢紊乱,减轻心肌纤维化程度,其机制可能与氧化应激介导的TGF-β 1/Smads信号通路有关.

Alcohol is a potent teratogen associated with dysmorphology, growth retardation, and neurological damage in children with the full fetal alcohol syndrome (FAS); alcohol is also associated with growth retardation and behavioral alterations in neonates prenatally exposed to various dosages. Questions remain about the long-term consequences of prenatal alcohol exposure. This study reports on the follow-up of a subsample of 68 children, the majority of whom were low income and black (mean age: 5 years, 10 months) who were first evaluated as neonates. Physical and cognitive outcomes of 25 children of women who drank throughout pregnancy [absolute alcohol (AA)/week: mean = 11.80 oz), even after receiving an educational intervention to stop drinking, were compared with outcomes of children in two contrast groups: a) women (n = 22) who stopped drinking (AA/week: mean = 11.46 oz) in the second trimester after an educational intervention but resumed postpartum; and b) women who did not drink during pregnancy and who drank little postnatally (n = 21). Children were compared for alcohol-related birth defects (ARBDs), growth (height, weight, and head circumference), and cognitive, academic, and adaptive measures. Neonatal and current physical measures were correlated to determine predictability of neonatal status. When the effects of age and gender were controlled, children in the continued-to-drink group showed significantly more ARBDs and had smaller head circumferences than those in the other two groups. When current drinking reported by caretakers was controlled, the children who were exposed throughout pregnancy also showed significant and consistent deficits in several areas of intellectual functioning including sequential processing (short-term memory and encoding) and overall mental processing. Alcohol-exposed children displayed significant deficits in preacademic skills when compared with children of nondrinkers, with both alcohol groups deficient in premath and reading skills. There were no differences in adaptive behavior at follow-up. These data suggest that alcohol exposure throughout pregnancy is correlated with persistent physical differences as well as identifiable deficits in sequential memory processes and specific academic skills. However, even when alcohol use is limited to the first part of pregnancy, significant deficits in academic skills and growth parameters are measurable.

为探讨肿瘤突变负荷(tumor mutation burden,TMB)对肝细胞癌(Hepatocellular carcinoma,HCC)患者预后的影响,从the Cancer Genome Atlas数据库下载357例HCC样本进行生物信息学分析.结果显示:在HCC患者中,C>T变异、错义突变及TP53基因突变频率最高;TMB与患者预后呈负相关(P<0.05).功能分析表明,差异基因富集于细胞外基质组织形成和硫化合物代谢途径(P<0.05).基于SFRP4、IL7R、FBLN2、COLEC10和CHGA基因,构建了HCC预后预测模型.结果表明,高危组患者1年、3年和5年预后较差(P<0.001).

Ginsenoside Rg1 is the active ingredient of the plant named genus Panax (ginseng), which exhibited significant bioactivities, including anti-inflammatory, antioxidation, and anti-diabetic effects. Herein, 4-week treatment of ginsenoside Rg1 remarkably decreased blood glucose levels and improved the resistance of insulin, oxidative stress, and inflammation along with lipid profile in T2D rats triggered via high-fat diet and streptozotocin (STZ). Ginsenoside Rg1 supplementation improved the intestinal microbial composition induced by type 2 diabetes (T2D), which increased the proportions of Lachnospiraceae_NK4A136_group and Lachnoclostridium and decreased the proportions of Lactobacillus . Additionally, Spearman's correlation test between the gut microflora and biomedical assays (| r | > .5) revealed that the Lachnospiraceae_NK4A136_group , Roseburia , and Romboutsia greatly affect intestinal microbiota, which may play pivotal roles in preventing T2D. Our findings illustrate the use of ginsenoside Rg1 as a dietary supplement along with prospective prebiotics due to its ability to alter the gut microflora and alleviate T2D-linked biochemical abnormalities. This was the first study to elucidate the influences of ginsenosides Rg1 in improving the intestinal microbiota of T2D in SD rats. The data illustrated that the ginsenosides Rg1 remarkably increased the proportions of SCFAs producing bacteria. Hence, ginsenoside Rg1 could be used as a potential prebiotic in the treatment of T2D through alteration of intestinal microbiota.

Diabetes cardiomyopathy has metabolic disorder and abnormality of cardiomyocytes, which is closely related to autophagy or apoptosis of cardiomyocytes. Scutellarin (SCU) is an important monomer extracted from Erigeron breviscapus (vant.) Hand.-Mazz. This study was conducted to investigate the function of SCU on apoptosis and autophagy of myocardial cells. We established a model of type 2 diabetic cardiomyopathy by high-fat and high-sugar diet. The results indicated that SCU downregulated blood glucose, total cholesterol (TC), triglyceride (TG), and low-density lipoprotein (LDL) levels and upregulated high-density lipoprotein (HDL) level. In addition, SCU downregulated lactic dehydrogenase 1 (LDH1) and creatine kinase (CK) levels. Meanwhile, SCU improved the myocardium morphology and reduced myocardial apoptosis. Furthermore, SCU promoted the mRNA and protein expression of autophagy-related factors (Beclin-1 and LC3-II) and inhibited the mRNA and protein expression of apoptosis-related factors (caspase-3, caspase-8, caspase-9, caspase-12, Bax, and Cyt-C). In conclusion, SCU can promote autophagy signal pathway by upregulating the autophagy-related factors and inhibit the apoptotic signal pathway by downregulating apoptosis-related factors, thereby relieving type 2 diabetic cardiomyopathy (T2DC).

目的 探讨灯盏乙素(SCU)抑制NOX(NOX2、NOX4)的表达,改善高脂高糖诱导的非酒精性脂肪性肝病(NAFLD)肝脏纤维化程度.方法 60只大鼠随机分为:正常组、模型组、SCU-25低剂量治疗组[25 mg/(kg·d)]、SCU-50 中剂量治疗组[50 mg/(kg·d)]SCU-100 高剂量治疗组[100 mg/(kg·d)]和姜黄素阳性药物治疗组[200mg/(kg·d)],每组10只.正常组给予普通饲料喂养24+8周,其余各组采用高脂高糖饲料喂养SD大鼠24周建立NAFLD动物模型后,给予不同浓度的SCU和姜黄素灌胃治疗8周.治疗完成后,称取大鼠的体重,麻醉状态下取大鼠血清和肝脏组织,称取肝脏的重量,计算肝脏指数;通过ELISA法检测血清和组织中ROS的含量;采用油红"0"染色检测肝脏组织脂质沉积,Masson染色检测肝脏组织的纤维化程度;Western blot和免疫组织化学法检测肝脏组织中NOX2、NOX4蛋白的表达.结果 模型组大鼠体重、肝重及肝脏指数增加(P＜0.01),不同剂量的SCU和姜黄素治疗后体重、肝重及肝脏指数降低,SCU-100高剂量治疗组和姜黄素阳性药物治疗组对体重和肝重降低的影响较为明显(P＜0.01).模型组血清和肝脏组织ROS含量增加(P＜0.01),不同剂量的SCU和姜黄素治疗后ROS含量降低(P＜0.05).在肝脏组织中,模型组出现大量的脂质沉积和组织的纤维化表现,不同剂量的SCU和姜黄素治疗后,脂质沉积减少,肝脏的纤维化程度改善.在肝脏组织细胞中,模型组的NOX2、NOX4蛋白表达上调(P＜0.05),不同剂量的SCU和姜黄素治疗后NOX2、NOX4的蛋白表达下调(P＜0.05),但剂量依赖不明显.结论 SCU可能通过抑制肝脏NOX2、NOX4蛋白的表达,降低ROS的产生,从而改善NAFLD的肝脏纤维化程度.

AimsNon-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease and lacks for safe and effective drug to therapy completely. Ginsenoside-Rg1 is one of the main components of ginseng and has been proved to counteract a variety of diseases. However, there is currently a lack of sufficient evidence to support the efficacy of ginsenoside-Rg1 in the treatment of NAFLD. Our aim was to investigate whether Ginsenoside-Rg1 is a potential drug for NAFLD.Main methodsNAFLD model in rats was established by giving a high-fat diet (HFD), ginsenoside-Rg1 was intragastrically administered 100 mg/kg/d for 8 weeks in NAFLD rat. Serum biochemical indices were measured. Liver tissues were stained with hematoxylin and eosin (HE) and oil red O. Total RNA was extracted from liver and was used for high throughput sequencing to identify the changes of transcriptome. The relevant hub genes were verified by quantitative real-time PCR and western blot.Key findingsSerum biochemical analysis indicated that ginsenoside-Rg1 improved liver function. Additionally, the staining of HE and oil red O indicated ginsenoside-Rg1 could remit pathology process of NAFLD. The transcriptome changes also support this result and reveals Atf3 and Acox2 were key genes.SignificanceTaken together, these results suggest that the efficiency of ginsenoside-Rg1 against NAFLD and confirmed that ginsenoside-Rg1 is a potential effective drug in treatment of NAFLD.

Objective To summarize the clinical characteristics of adult cases of paragonimiasis with lung masses as the main manifestation in Xishuangbanna, Yunnan Province, analyze the causes of misdiagnosis, and improve the levels of clinical diagnosis and treatment. Method We conducted a retrospective analysis of the clinical data and diagnosis and treatment of 8 adult cases of paragonimiasis with lung masses as the main manifestation that were diagnosed in the Oncology Department of People’s hospital of Xishuangbanna Dai Autonomous Prefecture from July 2014 to July 2019. Result All 8 patients were from epidemic paragonimiasis areas and had a confirmed history of consuming uncooked freshwater crabs. The clinical manifestations were mainly fever, dry cough, and chest pain. The disease durations were long, and peripheral blood eosinophil counts were elevated. The cases had been misdiagnosed as pneumonia or pulmonary tuberculosis. After years of anti-inflammatory or anti-tuberculosis treatment, the symptoms had not improved significantly. Patients eventually sought treatment from the oncology department for hemoptysis. Chest computed tomography showed patchy consolidation in the lungs, with nodules, lung masses, and enlarged mediastinal lymph nodes. Conclusion Paragonimiasis is a food-borne parasitic disease. Early clinical manifestations and auxiliary examination results are nonspecific. The parasite most often invades the lungs, and the resulting disease is often misdiagnosed as pneumonia, pulmonary tuberculosis, or lung cancer (Acta Trop 199: 05074, 2019). To avoid misdiagnosis, clinicians should inquire, in detail, about residence history and history of unclean food and exposure to infected water and make an early diagnosis based on the inquired information and imaging examination results. For patients who have been diagnosed with pneumonia or pulmonary tuberculosis and whose symptoms do not improve significantly after anti-inflammatory or anti-tuberculosis treatments, their epidemiological history should be traced to further conduct differential diagnosis and avoid misdiagnosis.