Structure Of Liver Tissue Research Articles

Immunometabolism of Liver Xenotransplantation and Prospective Solutions.

End-stage liver diseases, such as hepatocellular carcinoma or acute liver failure, critically necessitate liver transplantation. However, the shortage of available organ donors fails to meet the rapidly growing transplantation demand. Due to the high similarity of liver tissue structure and metabolism between miniature pigs and humans, xenotransplantation of pig livers is considered as a potentially viable solution to organ scarcity. In the 2024, teams from China first time have successfully transplanted a genetically modified Bama miniature pig liver into a clinically brain-dead man lasting for 10 days. This milestone in human xenotransplantation research not only confirms the feasibility of clinical application of xenotransplantation, but also underscores the daunting and protracted nature of this pathway. Despite advanced gene-editing technologies theoretically circumventing the occurrence of most transplant rejection reactions, patients still face challenges such as chronic immune rejection, coagulation disorders, and thrombotic microangiopathy after receiving xenografts. Moreover, prolonged use of immunosuppressive drugs may induce irreversible immune dysfunction, leading to opportunistic infections and metabolic disorders. This article compares the similarities and differences in livers between humans and pigs, summarizes the immunometabolism of xenotransplantation based on current findings, and provides research perspectives on pre-transplantation and post-transplantation strategies for prolonging the survival time of xenografts.

The synergistic effects of citicoline and silymarin on liver injury and thyroid hormone disturbances in γ-irradiated rats.

Exposure to ionizing radiation is inevitable due to its extensive use in industrial and medical applications. The search for effective and safe natural therapeutic agents as alternatives to chemical drugs is crucial to mitigate their side effects. This study aimed to evaluate the effects of citicoline as a standalone treatment or in combination with the anti-hepatotoxic drug silymarin in protecting against liver injury caused by γ-radiation in rats. The rats were exposed to γ-radiation (7Gy) and treated with citicoline (300mg/kg/day) and/or silymarin (50mg/kg/day). The results showed that citicoline alleviated liver damage in irradiated rats by reducing hepatic malondialdehyde levels, serum aspartate aminotransferase activity, and inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and nuclear factor-kappa B (NF-κB). It also increased acetylcholine (ACh) levels and the gene expression of the anti-inflammatory protein α7 nicotinic acetylcholine receptor (α7nAChR). Additionally, citicoline improved serum triiodothyronine (T3) levels, thyroid hormone receptor beta (TRβ) gene expression, and iodothyronine deiodinase type 1 activity in hepatic tissues of irradiated rats. Furthermore, citicoline enhanced the effects of silymarin on thyroxine (T4), TRβ, ACh, and α7nAChR when co-administered in irradiated rats. Histopathological analysis confirmed these findings, demonstrating improved liver tissue structure. Citicoline mitigates γ-radiation-induced liver damage by reducing oxidative stress, activating the cholinergic anti-inflammatory pathway, and modulating thyroid hormone metabolism. These findings support the use of citicoline as a safe standalone treatment or as an adjuvant with silymarin for managing liver damage and thyroid hormone disturbances caused by γ-irradiation.

Acute CCl4-induced intoxication reduces complex I, but not complex II-based mitochondrial bioenergetics - protective role of succinate.

The main therapeutic strategy for the treatment of patients with toxic liver failure is the elimination of the toxic agent in combination with the targeted mitigation of pathological processes that have been initiated due to the toxicant. In the current research we evaluated the strategy of metabolic supplementation to improve mitochondrial bioenergetics during acute liver intoxication. In our study, we have shown that acute CCl4-induced intoxication negatively affects Complex I (in the presence of glutamate-malate as energy substrates) based respiration, generation of mitochondrial membrane potential (ΔΨm), mitochondrial NAD(P)H pool and NADH redox index, mitochondrial calcium retention capacity (CRC) and structure and functions of the liver. Boosting of mitochondrial bioenergetics through the complex II, using succinate as metabolic substrate in vitro, significantly improved mitochondrial respiration and generation of ΔΨm, but not mitochondrial CRC. Co-application of rotenone along with succinate, to prevent possible reverse electron flow, didn't show significant differences compared to the effects of succinate alone. Treatment of animals with acute liver failure, using a metabolic supplement containing succinate, inosine, methionine and nicotinamide improved Complex I based respiration, generation of ΔΨm, mitochondrial NAD(P)H pool and NADH redox index, mitochondrial CRC and slightly decreased the level of oxidative stress. These changes resulted in averting destructive and dystrophic changes in the structure of rat liver tissue caused by CCl4 intoxication, concomitantly enhancing hepatic functionality. Thus, we propose that metabolic supplementation targeting complex II could serve as a potential adjunctive therapy in the management of acute liver intoxication.

Effects of Ammonia Stress on Liver Tissue Structure, Enzyme Activities, and Metabolome of Juvenile Largemouth Bass Micropterus salmoides.

Background: Ammonia, a ubiquitous contaminant in aquatic ecosystems, poses multifaceted threats to fish species at elevated concentrations. Methods: In order to investigate the toxic effects of chronic ammonia stress on the liver of juvenile Micropterus salmoides, the present experiment was conducted to investigate the differences in changes in liver tissue structure, enzyme activities, and metabolomes after 28 days of ammonia exposure (0, 4, 8, and 16 mg/L). Results: The findings revealed that ammonia exposure induced significant oxidative stress in the liver, manifesting in decreased activities of antioxidant enzymes SOD and GSH-Px, elevated levels of GSH, GST, and MDA, and heightened activities of immune enzymes LZM, ALP, and ACP. An increase in ammonia concentration exacerbated liver tissue damage. Metabolome analysis further unveiled perturbations in liver metabolites of Micropterus salmoides exposed to ammonia, with Ala-His emerging as a potentially pivotal functional substance under chronic stress. Specifically, the 4 mg/L group responded to ammonia toxicity by augmenting GSH and L-Carnosine levels, the 8 mg/L group detoxified via upregulation of L-Glutamine, and the 16 mg/L group mitigated toxicity through the urea synthesis pathway. Conclusions: This research offers preliminary insights into the toxicological responses of Micropterus salmoides under chronic ammonia stress. It is suggested that the duration of ammonia concentration exceeding 4 mg/L in high-density aquaculture should not exceed 7 days.

Quercetin Promotes the M1-to-M2 Macrophage Phenotypic Switch During Liver Fibrosis Treatment by Modulating the JAK2/STAT3 Signaling Pathway.

To investigate the underlying mechanism by which quercetin (Que) regulates macrophage polarization and its subsequent therapeutic effect on liver fibrosis, an important pathological precondition for hepatocellular carcinoma (HCC). In vitro experiments were performed on the RAW264.7 mouse macrophage line. After the induction of M1-type macrophages with LPS, the effects of Que on cell morphology, M1/M2 surface marker expression, cytokine expression, and JAK2/STAT3 expression were analyzed. In vivo, male SD rats were used as a model of CCL4-induced hepatic fibrosis, and the effects of Que on serum aminotransferase levels, the histopathological structure of liver tissues, and macrophage-associated protein expression in liver tissues were analyzed. In vitro experiments revealed that Que can suppress the activation of the JAK2/STAT3 signaling pathway, leading to decreases in the expression of M1 macrophage surface markers and cytokines. Additionally, Que was found to increase the expression of M2 macrophage surface markers and cytokines. In vivo, assays demonstrated that Que significantly ameliorated the development of inflammation and fibrosis in a rat liver fibrosis model. Que can inhibit hepatic fibrosis by promoting M1 to M2 macrophage polarization, which could be associated with its ability to suppress the JAK2/STAT3 signaling pathway in macrophages.

Protective effect of Zhizi Huangqi Shanzha formula on aflatoxin poisoning in mice and its effect on intestinal flora.

To evaluate the protective effect of Zhizi Huangqi Shanzha formula (, ZHSF) on aflatoxin-induced liver injury. The protective effect of ZHSF on the aflatoxin-induced liver injury was evaluated by histological observation, blood cell analysis, evaluation of liver function and immunity, and gut microbiota analysis. ZHSF can significantly up-regulate the percentage of lymphocytes and eosinophils in the blood of Aflatoxin B1-intoxicated mice, down-regulate the levels of serum aspartate aminotransferase, alanine aminotransferase, and malondialdehyde, and recover the liver tissue structure. Aflatoxin poisoning induces a variation of the intestinal flora of mice, and ZHSF may recover the variation of intestinal flora induced by Aflatoxin B1. Cluster analysis showed that the intestinal flora of mice in the intervention group was more similar to that of the control group. Correlation analysis showed that Lachnospiraceae, Desulfovibrio, and Lactobacillus may be the key flora for the pharmacological effects of ZHSF. ZHSF may protect against aflatoxin-induced liver damage, improve immunity, and inhibit oxidative stress by regulating the composition and relative abundance of intestinal flora, which makes it a promising liver-protective candidate drug.

Anticancer Effects of Vaccinium arctostaphylos L. through HOTAIR/miR-124/Notch1 Axis of Hepatocellular Carcinoma in Rat: A Biochemical, Molecular, Immunohistochemical, and Histopathological Approaches

Background and Purpose We investigated the effectiveness of Vaccinium arctostaphylos L. fruit extract (VAFE) in protecting hepatocytes against N-diethylnitrosamine (DEN)-related hepatocellular carcinoma (HCC) by exploring its impact on biochemical, molecular, and antioxidant pathways, as well as its role in regulating the HOTAIR/miR-124/Notch1 axis pathway. Materials and Methods In the present study, 50 Wistar rats in 5 groups ( n = 10/group) of normal, HCC (80 mg/kg DEN), HCC rats receiving 200 and 400 mg/kg DEN + VAFE, and normal rats receiving 400 mg/kg VAFE were divided. The serum concentrations of liver function indices (bilirubin, total protein, albumin, alanine aminotransferase, aspartate aminotransferase, C-reactive protein, and alkaline phosphatase), inflammatory cytokines (interleukin (IL)-1β, IL-10, tumor necrosis factor-α, and IL-6) and oxidants parameters (catalase, superoxide dismutase, and glutathione peroxidase enzyme activity and nitric oxide levels) were measured. Liver tissue HOTAIR, miR-124, Notch1, and Jagged1 genes and proteins were measured. p53-positive cells of liver hepatocytes were evaluated by immunohistochemical technique. Results DEN induced significant changes in body and liver weight, serum liver enzymes, antioxidant levels, inflammatory markers, and HOTAIR/miR-124/Notch1 axis genes/proteins expression related to liver pathways. VAFE demonstrated dose-dependent effects in countering these changes, significantly improving weight, liver health, antioxidant capacity, and inflammatory responses, especially at 400 mg/kg. The histopathological evaluation showed improvements in liver tissue structure with VAFE treatment. Conclusion Overall, our study demonstrates the administration of VAFE can anticancer effects of DEN-induced HCC.

Toxicity of Local Natural Ingredients from East Java, Indonesia Yam Bean (Pachyrhizus erosus) and Avocado (Persea americana Mill) on the Liver and Kidney Structure of Sprague Dawley Rats

Aims: The aim of the research was to test the toxicity of jicama (Pachyrhizus erosus) and avocado (Persea americana Mill) on the structure of liver and kidney tissue in Sprague Dawley rats. Study Design: Male Sprague Dawley rats aged 5 months, 24 animals. Treatment of synthetic and natural ingredients. 6 treatment groups were given daidzein (P1), 6 treatment groups were given niacin (P2), 6 treatment groups were given jicama (Pachyrhizus erosus) (P3) and 6 treatment groups were given avocado (Persea americana Mill) (P4). Each treatment was carried out for 28 days. On the 29th day, surgery was performed and the liver and kidneys were removed, followed by HE staining. Result: The results showed that the structure of liver and kidney tissue given daidzein and niacin experienced necrosis, increased vascularization, hemorrhage and fatty degeneration. Conclusion: The use of natural ingredients does not produce toxic (harmful) effects in the body compared to synthetic substances. The percentage of kidney necrosis with daidzein administration is 24%, and with niacin administration, it is 29%. The percentage of liver necrosis with daidzein administration is 20%, and with niacin administration, it is 24%.

Exploring the Antitumour Potential of <i>Diospyros chloroxylon</i> Roxb. Extract in EAC Models: An Integrative <i>In Vitro</i> and <i>In Vivo</i> Approach

Background: Natural compounds have emerged as promising alternatives, owing to their low toxicity and potential efficacy. This study investigates the anticancer effects of Diospyros chloroxylon Roxb. leaf extract on Ehrlich Ascites Carcinoma (EAC) in vitro and in vivo. Methods: The in vitro cytotoxicity of D. chloroxylon extract was assessed using the MTT assay on various cancer cell lines, including EAC, A549 (lung), MCF-7 (breast), DU 145 (prostate), HT 29 (colon) and Human Umbilical Vein Endothelial Cells (HUVECs). The in vivo study involved the treatment of EAC-bearing mice with two doses (200mg/kg and 400mg/kg). Parameters such as body weight, tumour volume, packed cell volume, viable and non-viable cell counts, mean survival time and lifespan were evaluated. Haematological parameters and biochemical markers were also analysed, followed by histopathological analysis. Results: In the MTT assay, D. chloroxylon extract showed selective cytotoxicity, exhibiting a strong effect on EAC cells with lower IC50 values than other cancer cell lines and minimal toxicity towards HUVECs. In in vivo, D. chloroxylon treatment mitigated weight loss, reduced tumour volume in a dose-dependent manner and improved survival times. It also normalised haematological and biochemical parameters, indicating its potential to manage cancer-induced complications. Histopathological studies showed that doxorubicin and higher doses of D. chloroxylon enhanced liver tissue structure. However, complete recovery from EAC-induced hepatic alterations, such as dilated sinusoids, remains elusive. Conclusion: Diospyros chloroxylon Roxb. leaf extracts demonstrated significant anticancer activity in vitro and in vivo. Its ability to selectively induce cytotoxic effects on cancer cells and its beneficial effects in an EAC mouse model suggests its potential as a therapeutic agent for cancer treatment.

Lactiplantibacillus plantarum N4 ameliorates lipid metabolism and gut microbiota structure in high fat diet-fed rats.

Lowing blood lipid levels with probiotics has good application prospects. This study aimed to isolate probiotics with hypolipidemic efficacy from homemade na dish and investigate their mechanism of action. In vitro experiments were conducted to determine the cholesterol-lowering ability of five isolates, with results showing that Lactiplantibacillus plantarum N4 exhibited a high cholesterol-lowering rate of 50.27% and significant resistance to acid (87%), bile salt (51.97%), and pepsin (88.28%) in simulated gastrointestinal fluids, indicating promising application prospects for the use of probiotics in lowering blood lipids. The findings from the in vivo experiment demonstrated that the administration of N4 effectively attenuated lipid droplet accumulation and inflammatory cell infiltration in the body weight and liver of hyperlipidemic rats, leading to restoration of liver tissue morphology and structure, as well as improvement in lipid and liver biochemical parameters. 16S analysis indicated that the oral administration of N4 led to significant alterations in the relative abundance of various genera, including Sutterella, Bacteroides, Clostridium, and Ruminococcus, in the gut microbiota of hyperlipidemia rats. Additionally, fecal metabolomic analysis identified a total of 78 metabolites following N4 intervention, with carboxylic acids and their derivatives being the predominant compounds detected. The transcriptomic analysis revealed 156 genes with differential expression following N4 intervention, leading to the identification of 171 metabolic pathways through Kyoto Encyclopedia of Genes and Genomes enrichment analysis. Notably, the glutathione metabolism pathway, PPAR signaling pathway, and bile secretion pathway emerged as the primary enrichment pathways. The findings from a comprehensive multi-omics analysis indicate that N4 influences lipid metabolism and diminishes lipid levels in hyperlipidemic rats through modulation of fumaric acid and γ-aminobutyric acid concentrations, as well as glutathione and other metabolic pathways in the intestinal tract, derived from both the gut microbiota and the host liver. This research offers valuable insights into the therapeutic potential of probiotics for managing lipid metabolism disorders and their utilization in the development of functional foods.

LncRNA FRMD6-AS1/miR-491-5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis.

Liver fibrosis is an invertible pathophysiologic process featured by excessive accumulation of extracellular matrix (ECM) which injures liver cells and activates hepatic stellate cells (HSCs). Besides, inducing ferroptosis in activated HSCs can alleviate liver fibrosis. LncRNAs modulate ferroptosis in activated HSCs and ECM deposition in liver fibrosis. However, the role of lncRNA FRMD6-AS1 in liver fibrosis is not discovered. In this study, lncRNA FRMD6-AS1 was dramatically up-regulated in activated HSCs. Knockdown of FRMD6-AS1 markedly increased iron ion, ROS and MDA levels, decreased GSH level, SLC7A11 and GPX4 protein expressions in activated HSCs. In addition, HSCs activation markers α-SMA and COL1α1 expressions were up-regulated in activated HSCs; knockdown of FRMD6-AS1 markedly down-regulated α-SMA and COL1α1 expressions in HSCs. Besides, lncRNA FRMD6-AS1 could interact with miR-491-5p, and negatively modulate miR-491-5p expression. USP13 was a target of miR-491-5p, and could be negatively modulated by miR-491-5p. Moreover, FRMD6-AS1 knockdown increased iron ion and ROS levels, decreased SLC7A11 and GPX4 protein expressions, facilitated HSCs viability, and up-regulated α-SMA and COL1α1 expressions via miR-491-5p/USP13 pathway. Finally, FRMD6-AS1 knockdown restored liver tissue structure and abrogated fibrosis in livers in a CCL4 liver fibrosis mouse model. Hence, lncRNA FRMD6-AS1/miR-491-5p/USP13 pathway repressed ferroptosis, promoted ECM deposition and facilitated liver fibrosis in vitro and in vivo models.

Anti-obesity and other health benefits of bioprocessed black rice bran in combination with green tea extract in 3T3-L1 preadipocyte cells and in mice on a high-fat diet.

Black rice bran, a waste product from the commercial milling of black rice that removes the bran and germ leaving the starchy endosperm, contains bioactive anthocyanin, phenolic, and phytosteroid compounds that may have health benefits. This study determined the effect of a polysaccharide-rich bioprocessed (fermented) black rice bran and a green tea extract individually and in combination on weight loss in orally fed mice on a high-fat diet and on concurrent changes in blood glucose and insulin as well as in cholesterol, triglyceride, and high-density and low-density lipoproteins (HDL and LDL). At the end of the eight-week feeding study, the combination diet resulted in a 67% lower weight gain than mice on a high-fat diet alone, a greater effect than that of bioprocessed black rice bran or green tea extract individually. The weight loss caused by the combination diet seems to be the result of decreased dietary efficiency. The observed trends in the glucose and insulin data suggest that the combined diet also has anti-diabetic properties, and the corresponding trends in the levels of the serum lipoproteins suggest that the combined diet might also protect against heart disease. Effects on the content, structure, and function of white adipose and liver tissues and on obesity-related biomarkers support the trends in the weight loss data. Based on the observed beneficial effects in 3T3-L1 pre-adipocyte cells and mice, we suggest the need to investigate if the new multifunctional combination food product can also protect against obesity and chronic diseases in humans. Mechanistic aspects that govern the anti-obesity effects and suggestions for future research are discussed.

Использование экстракта Laminariacolax aecidioides при выращивании молоди африканского клариевого сома

An assessment was made of growth dynamics, hematological parameters of peripheral blood and changes in the structure of intestinal and liver tissues of juvenile African catfish Clarias gariepinus when an aqueous extract from the marine brown alga Laminariocolax aecidioides was included in the feed. Shown that the addition of an algal extract at a concentration of 5 % led to a significant improvement in the growth performance of individuals, which was expressed in an increase in growth rate, a decrease in the feed ratio and an increase in the fatness of fish. According to the results of hematological and histological studies, the extract of L. aecidioides contributed to the modulation of fish immunity by increasing the content of granulocytes (basophils and neutrophils) in the blood, as well as activation of the secretory function of the intestine (thickening of the lamina propria) and the immune function of the intestinal mucosa (increase in the size of goblet cells and an increase in the occurrence of clusters of eosinophilic and interepithelial cells). At the same time, the algae additive from L. aecidioides had virtually no negative effect on the histological picture of fish liver.

Itraconazole halts hepatocellular carcinoma progression by modulating sonic hedgehog signaling in rats: A novel therapeutic approach

Liver cancer stands as the fourth leading global cause of death, and its prognosis remains grim due to the limited effectiveness of current medical interventions. Among the various pathways implicated in the development of hepatocellular carcinoma (HCC), the hedgehog signaling pathway has emerged as a crucial player. Itraconazole, a relatively safe and cost-effective antifungal medication, has gained attention for its potential as an anticancer agent. Its primary mode of action involves inhibiting the hedgehog pathway, yet its impact on HCC has not been elucidated. The main objective of this study was to investigate the effect of itraconazole on diethylnitrosamine-induced early-stage HCC in rats. Our findings revealed that itraconazole exhibited a multifaceted arsenal against HCC by downregulating the expression of key components of the hedgehog pathway, shh, smoothened (SMO), and GLI family zinc finger 1 (GLI1), and GLI2. Additionally, itraconazole extended survival and improved liver tissue structure, attributed mainly to its inhibitory effects on hedgehog signaling. Besides, itraconazole demonstrated a regulatory effect on Notch1, and Wnt/β-catenin signaling molecules. Consequently, itraconazole displayed diverse anticancer properties, including anti-inflammatory, antiangiogenic, antiproliferative, and apoptotic effects, as well as the potential to induce autophagy. Moreover, itraconazole exhibited a promise to impede the transformation of epithelial cells into a more mesenchymal-like phenotype. Overall, this study emphasizes the significance of targeting the hedgehog pathway with itraconazole as a promising avenue for further exploration in clinical studies related to HCC treatment.

The Mechanism Underlying the Hypoglycemic Effect of Epimedin C on Mice with Type 2 Diabetes Mellitus Based on Proteomic Analysis.

Type 2 diabetes mellitus (T2DM) has become a worldwide public health problem. Epimedin C is considered one of the most important flavonoids in Epimedium, a famous edible herb in China and Southeast Asia that is traditionally used in herbal medicine to treat diabetes. In the present study, the therapeutic potential of epimedin C against T2DM was ascertained using a mouse model, and the mechanism underlying the hypoglycemic activity of epimedin C was explored using a label-free proteomic technique for the first time. Levels of fasting blood glucose (FBG), homeostasis model assessment of insulin resistance (HOMA-IR), and oral glucose tolerance, as well as contents of malondialdehyde (MDA) and low-density lipoprotein cholesterol (LDL-C) in the 30 mg·kg-1 epimedin C group (EC30 group), were significantly lower than those in the model control group (MC group) (p < 0.05), while the contents of hepatic glycogen, insulin, and high-density lipoprotein cholesterol (HDL-C), as well as activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the EC30 group were notably higher than those in the MC group (p < 0.05). The structures of liver cells and tissues were greatly destroyed in the MC group, whereas the structures of cells and tissues were basically complete in the EC30 group, which were similar to those in the normal control group (NC group). A total of 92 differentially expressed proteins (DEPs) were enriched in the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. In the EC30 vs. MC groups, the expression level of cytosolic phosphoenolpyruvate carboxykinase (Pck1) was down-regulated, while the expression levels of group XIIB secretory phospholipase A2-like protein (Pla2g12b), apolipoprotein B-100 (Apob), and cytochrome P450 4A14 (Cyp4a14) were up-regulated. According to the KEGG pathway assay, Pck1 participated in the gluconeogenesis and insulin signaling pathways, and Pla2g12b, Apob, and Cyp4a14 were the key proteins in the fat digestion and fatty acid degradation pathways. Pck1, Pla2g12b, Apob, and Cyp4a14 seemed to play important roles in the prevention and treatment of T2DM. In summary, epimedin C inhibited Pck1 expression to maintain FBG at a relatively stable level, promoted Pla2g12b, Apob, and Cyp4a14 expressions to alleviate liver lipotoxicity, and protected liver tissues and cells from oxidant stress possibly by its phenolic hydroxyl groups.

Role of fallopia plant extraction in induced hepatocellular carcinoma.

In 2020, around 19.3 million new cancer cases resulted in 3.5 million deaths. It is estimated that there will be 28.4 million cases by 2040. Plant-derived natural products, such as alkaloids, flavonoids, terpenoids, and phenolic compounds, offer a wide range of chemical structures and biological activities that can be explored for their potential in cancer research. In a particular study, researchers investigated the potential anticancer effects of Fallopia flower extracts on cancer induced by TAA (a carcinogen). They examined the extracts to identify specific amino acids with antioxidant properties and assessed their impact on liver function and tissue structure. The results showed that the plant extracts had positive effects on the histological section of the TAA-treated group. Additionally, the group of male rats treated with TAA and a chemotherapy drug called MMC displayed positive effects. Similarly, the group of male rats treated with TAA, flower plant extract, and MMC also showed positive effects. These findings suggest that the extract from Fallopia flowers could be considered as a traditional therapy with potential anticancer properties.

Effects of Vitamin E on Immune Response, Antioxidant Capacity, and Liver Tissue Structure of Crucian Carp under Acute Cold Stress

The purpose of this study was to investigate the effects of vitamin E addition to the water column on immune response, antioxidant capacity, and liver tissue structure of crucian carp (Carassius auratus) under acute cold stress. Crucian carp was placed in the aqueous solution of control group (E1), negative control group (E2), and 100 mg/L vitamin E (E3) and cooled from 20 to 5°C by cold acclimation intelligent cooling device. Samples were taken at three temperature points of 20, 10, and 5°C, respectively, and the samples were detected and analyzed. The results showed that the content of each index increased under acute cold stress. The contents of white blood cell, red blood cell, hemoglobin, platelet, lysozyme, and glutathione peroxidase in E3 treatment group were significantly lower than those in E1 and E2 treatment groups ( P &lt; 0.05 ). The contents of cholinesterase, alkaline phosphatase, acid phosphatase, hydrogen peroxide, superoxide anion, superoxide dismutase, peroxidase, and malondialdehyde in E3 treatment group were significantly lower than those in E1 and E2 treatment groups ( P &lt; 0.01 ). Under acute cold stress, the liver tissue structure of crucian carp also changed, such as hepatocyte vacuolization, and the damage degree of E3 treatment group was lower than that of E1 and E2 treatment groups. In summary, the addition of vitamin E in water to treat crucian carp can reduce the harm caused by acute cold stress to its body and provide a theoretical reference for the application of vitamin E in water to alleviate fish stress.

The Effect of Diabetes Mellitus Type 1 on the Energy Metabolism of Hepatocytes: Multiphoton Microscopy and Fluorescence Lifetime Imaging

A decrease in the regenerative potential of the liver during the development of non-alcoholic fatty liver disease (NAFLD), which is observed in the vast majority of patients with diabetes mellitus type 1, significantly increases the risk of postoperative liver failure. In this regard, it is necessary to develop new approaches for the rapid intraoperative assessment of the condition of liver tissue in the presence of concomitant liver pathology. A modern label-free approach based on multiphoton microscopy, second harmonic generation (SHG), and fluorescence lifetime imaging microscopy (FLIM) allow for the evaluation of the structure of liver tissue as well as the assessment of the metabolic state of hepatocytes, even at the cellular level. We obtained optical criteria and identified specific changes in the metabolic state of hepatocytes for a reduced liver regenerative potential in the presence of induced diabetes mellitus type 1. The obtained criteria will expand the possibilities for the express assessment of the structural and functional state of liver tissue in clinical practice.

Total Astragalus saponins can reverse type 2 diabetes mellitus-related intestinal dysbiosis and hepatic insulin resistance in vivo.

Intestinal flora homeostasis in rats with type 2 diabetes mellitus (T2DM) was evaluated to explore the effects of total Astragalus saponins (TAS) on hepatic insulin resistance (IR). Six-week-old male Sprague-Dawley rats were fed high-fat and high-sugar diet for 4 weeks and intraperitoneally injected with streptozotocin to induce T2DM, and they were then randomly divided into control, model, metformin, and TAS groups. Stool, serum, colon, and liver samples were collected after 8 weeks of drug administration for relevant analyses. TAS reduced fasting blood glucose, 2-hour postprandial blood glucose, area under the curve of oral glucose tolerance test, glycated serum protein, homeostasis model assessment of insulin resistance, total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels in T2DM rats but increased insulin, C-peptide, and high-density lipoprotein cholesterol levels. Moreover, TAS improved the morphology and structure of liver and colon tissues and improved the composition of the intestinal microbiome and bacterial community structure at different taxonomic levels. In addition, TAS increased the protein expression of hepatic IRS-1, PI3K, PDK1, and p-AKT and decreased the protein expression of p-GSK-3β. Meanwhile, TAS increased the mRNA expression of liver PDK1, PI3K, and GS and decreased the mRNA expression of GSK-3β. TAS can ameliorate T2DM-related abnormal glucose and blood lipid metabolism, intestinal dysbiosis, and IR.

Effects of adding whole barley flour to bread and its impact on anti-obesity action of female rats fed a high-fat diet

The present investigation was focused on the effect of whole barley on balady bread properties and its nutritional and biological evaluation through different sets of rats. Chemical, sensorial and microbial properties were determined. The anti- obesity action of high levels of whole barley 60, 80% supplemented bread through 30 female rats evaluated. The increasing level of whole barley flour (WBF) incorporated into bread significantly increased crude fiber and ash contents High levels from WBF led to decrease the microbial load in the bread. Concerning biological evaluation, body weight gain of groups treated with barley had a significant decrease. Nearly all fatty cells from group 5 treated with bread (80% WBF) are small like negative group as demonstrated by histopathology of fatty tissue. Barley bread stabilized blood glucose levels, ameliorated lipid profile, liver enzymes and urea level but creatinine level was in similar level and improved the histological structure of liver tissues. In conclusion, this study demonstrates that incorporating high levels of whole barley into balady bread not only enhances its nutritional and microbial properties but also exerts anti-obesity effects and promotes overall metabolic health in rats. These findings highlight the potential of barley-supplemented bread as a functional food product with various health benefits. These findings highlight the potential of barley-supplemented bread as a functional food product with various health benefits.