ObjectiveTo explore the effects of Total Flavonoids from Litchi Seed on the expression of differential lncRNAs and mRNAs in liver fibrosis rats using high-throughput sequencing technology and to analyze its biological functions.MethodsExperiments was conducted at the experimental animal center of Guangxi University of Chinese Medicine from April 2021 to July 2021.A rat model of liver fibrosis was established, with rats randomly assigned to the control group(Control), model group(Model), and Total Flavonoids from Litchi Seed group(TFL). The TFL group was administered 50mg·kg-1·d-1of TFL for a total of 6 weeks. HE and Masson staining were used to observe liver tissue fibrosis changes. Serum levels of hyaluronidase(HA), type IV collagen(Ⅳ-C), laminin(LN), and type III procollagen(PC III) were measured using ELISA. RNA-seq high-throughput sequencing technology was used to identify differentially expressed lncRNAs and mRNAs between the Model and TFL groups. The cis method was used to predict target genes of differentially expressed lncRNAs. GO and KEGG analyses were conducted for biological function enrichment of the differentially expressed lncRNAs target genes and mRNAs.ResultsCompared with the Model group, the TFL group exhibited a significant decrease in liver fibrosis score(F=14.420,P<0.001) and serum levels of HA, Ⅳ-C, LN, and PC-Ⅲ(F=47.055, 74.655, 177.328, 54.445,P<0.001). A total of 73 differentially expressed lncRNAs(43 up-regulated, 30 down-regulated) were identified between the Model and TFL groups, along with 261 differentially expressed mRNAs(150 up-regulated, 111 down-regulated). Using the cis method, 24 target genes were predicted between the Model and TFL groups. Biological function enrichment analysis indicated that TFL plays an anti-liver fibrosis role by participating in signaling pathways such as circadian rhythm, glutathione metabolism, ubiquinone, and pentose phosphate.ConclusionTFL significantly improved the pathological morphology of fibrotic tissue in rats, reduced serum levels of HA, Ⅳ-C, LN, and PC-III, and exerted an anti-liver fibrosis effect. The mechanism of action may involve regulating the expression of specific differential lncRNAs and mRNAs and participating in signaling pathways such as circadian rhythms, glutathione metabolism, ubiquinone, and pentose phosphate.

ObjectiveTo investigate the effect and possible mechanism of the drug hirudin on hypoxia induced human microvascular endothelial cells(HCMECs) mesenchymal transition(EndMT).MethodsHCMECs cells cultured conventionally were randomly divided into control group, Hypoxia group and Hirudin group. The control group was routinely cultured without any treatment. The hypoxic group was placed in a hypoxic incubator for 72h, and the Hirudin group was pre-added with Hirudin working solution, and then placed in a hypoxic incubator for 72h after 4h. The proliferation capacity of HCMECs was detected by MTS colorimetry. The morphology of HCMECs was observed by inverted microscope. Immunofluorescence identification of HCMECs interstitial trans differentiation, Western Blot detection of endothelial interstitial trans differentiation related proteins: Endothelial cells labeled platelet endothelial cell adhesion molecule(PECAM-1/CD31) and vascular endothelial cadherin(VE-cadherin), and stromal cells labeled α smooth muscle actin(α-SMA) and fibroblast specific protein 1(FSP-1). And the expression of hypoxia inducible factor-1α(HIF-1α), transforming growth factor β1(TGF-β1), Smad homology 2/3(Smad2/3), Zinc finger transcription factor(snail) related signaling pathways.ResultsMTS showed that hypoxia significantly inhibited cell activity(P<0.01), and the cell activity was strongest when hirudin concentration was 100μg/ml(P<0.01). After 72h of cell culture in each group, the cells in the control group showed a pave-like or pebble-like structure under an inverted microscope, while the cells in the hypoxic group changed from pebble-like structure to dispersed long spindle shape, close to the shape of fibroblasts. Western Blot and immunofluorescence results showed: Compared with the normal group, the protein levels of CD31 and VE cadherin in hypoxia group were decreased(P<0.01), and the expression of vWF was decreased. α-SMA and FSP-1 protein levels increased(P<0.01) and vimentin expression was enhanced. Compared with hypoxia group, hirudin significantly increased the expression of CD31 and VE-cadherin(P<0.01), enhanced the expression of vWF, and down-regulated α-SMA. The expression of FSP-1 protein(P<0.01) decreased the expression of vimentin. Compared with the control group, hypoxic group of TGF-β1, HIF-1α, p smad2/3, snail protein expression(P<0.01) were higher, than to the hypoxia group, Cut HIF-1α, hirudin TGF-β1, p smad2/3, snail protein expression(P<0.01).ConclusionHirudin can improve hypoxia induced EndMT in HCMECs cells, and the mechanism may be related to HIF-α/TGF-β1/smad/snail pathway.

Collaterals disease theory is an academic theory that studies the state of pathogenesis in miscellaneous diseases due to internal injury and severe exogenous diseases and the treatment based on syndrome differentiation. The pathogenesis of post infectious bronchiolitis obliterans in children conforms to the theoretical connotation of collaterals disease theory. Children's physical weakness, thinning of the lung collaterals and disharmony of nutrient qi and defensive qi are the root of the disease; exogenous pathogenic factors that enters the interior, the depressed lung qi and phlegm and blood stasis blocking collaterals are the disease-causing mechanism; the unresolved pathogenic factors, the undamaged qi and yin and the injury to the lung's collaterals are the root of the reoccurrence. Combined with the academic idea of preventive treatment of disease, the staging prevention and treatment of post infectious bronchiolitis obliterans is discussed in terms of Collaterals disease theory.

Sarcopenia, an age related disease characterized by loss of skeletal muscle mass and function, is considered an emerging complication in older patients with type 2 diabetes mellitus(T2DM). T2DM accelerates the loss of muscle mass and function, while sarcopenia can lead to disrupted glucose metabolism, reduced physical activity, and an increased risk of diabetes. However, the specific mechanisms involved between T2DM and sarcopenia have not been thoroughly investigated. Therefore, this review aims to explore the pathophysiological mechanisms and treatment strategies associated with sarcopenia and diabetes in order to improve the quality of life and reduce the occurrence of related complications in elderly people with diabetes.

Nonalcoholic fatty liver disease(NAFLD) is a common disease that causes abnormal liver function. It is usually caused by various reasons that weaken the liver's ability to metabolize fat, making it difficult to metabolize the intake of lipid substances normally, resulting in excessive deposition of fat in the liver. This has been characterized as a global public health challenge event. The prevalence of NAFLD is on the rise globally, affecting 20% to 45% of the general population. There is currently no approved treatment plan for the progression of the disease or the development of liver cirrhosis or hepatocellular carcinoma. With the expansion of clinical research on NAFLD, it has been found that it is closely related to Helicobacter pylori(Hp) infection. This article reviews the research progress on the mechanism of Hp infection in NAFLD, providing new methods for the clinical prevention and treatment of NAFLD.