Cornus officinalis with high pressure wine steaming enhanced anti-hepatic fibrosis: Possible through SIRT3-AMPK axis.

Cornus officinalis, a medicinal and edible plant known for its liver-nourishing properties, has shown promise in inhibiting the activation of hepatic stellate cells (HSCs), crucial indicators of hepatic fibrosis, especially when processed by high pressure wine steaming (HPWS). Herein, this study aims to investigate the regulatory effects of cornus officinalis, both in its raw and HPWS forms, on inflammation and apoptosis in liver fibrosis and their underlying mechanisms. In vivo liver fibrosis models were established by subcutaneous injection of CCl4, while in vitro HSCs were exposed to transforming growth factor-ß (TGF-ß). These findings demonstrated that cornus officinalis with HPWS conspicuously ameliorated histopathological injury, reduced the release of proinflammatory factors, and decreased collagen deposition in CCl4-induced rats compared to its raw form. Utilizing ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometer (UHPLC-QTOF-MS) combined with network analysis, we identified that the pharmacological effects of the changed components of cornus officinalis before and after HPWS, primarily centered on the adenosine phosphate (AMP)-activated protein kinase (AMPK) pathway. Of note, cornus officinalis activated AMPK and Sirtuin 3 (SIRT3), promoting the apoptosis of activated HSCs through the caspase cascade by regulating caspase3, caspase6 and caspase9. siRNA experiments showed that cornus officinalis could regulate AMPK activity and its mediated-apoptosis through SIRT3. In conclusion, cornus officinalis exhibited the ability to reduce inflammation and apoptosis, with the SIRT3-AMPK signaling pathway identified as a potential mechanism underlying the synergistic effect of cornus officinalis with HPWS on anti-liver fibrosis.

Evaluate the clinical efficacy of traditional Chinese Medicine as the neoadjuvant treatment in reducing the incidence of hepatocellular carcinoma in patients with hepatitis B-related cirrhosis: A systematic review and meta-analysis.

Background: Traditional Chinese Medicine (TCM), has been used for hepatocellular carcinoma (HCC) at every therapeutic stage, even before tumor formation. However, the efficacy of TCM in reducing the incidence of HCC in patients with chronic hepatitis B-related cirrhosis remains unclear. This study aims to address this gap. Methods: Publications were collected from PubMed, EMBASE, Cochrane Library, Web of Science, CNKI, Sino Med, VIP, and Wan Fang Databases. Relative risk (RR) was calculated with a 95 % confidence interval (CI). Heterogeneity was assessed. The Cochrane Collaboration's tool was used to assess the risk of bias. Results: 10 studies with 2702 patients showed that the combination therapy significantly reduced the incidence of HCC in patients with post-hepatitis B cirrhosis at 1, 3, and 5 years. However, the preventive effects of TCM were in compensated cirrhosis, but not the decompensated cirrhosis. Furthermore, TCM correlated with improved liver function and enhanced virological response. Conclusion: Combination therapy with TCM demonstrated the certain potential in reducing the incidence of HCC in patients with hepatitis B cirrhosis. This is attrinuted to the improvement of liver function and enhancement of the viral response. However, the efficacy of TCM in the field still needs more high-quality RCTs to provide stronger evidence in the future.

Self-heating mitochondrion-induced free radical blast for immunogenic cell death stimulation and HCC immunotherapy.

Hepatocellular carcinoma (HCC) is an immunosuppressive tumor associated with high mortality. Photothermal and photodynamic therapies have been applied to induce immunogenic cell death (ICD) in HCC, successfully eliciting immune responses but facing limitations in penetration depth in clinical trials. Here, intrinsic mitochondrial hyperthermia was used to trigger thermosensitive drug release. The mitochondria were further self-heated through 2,4-dinitrophenol uncoupling, dramatically promoting free radical initiation and inducing tumor ICD. The synthesized mitochondrial-targeting TPP-HA-TDV nanoparticles specifically generated free radicals in the mitochondria without external stimulation, and obviously enhanced the release of ICD markers, subsequently evoking immune responses. The results showed that mitochondrial hyperthermia could be an endogenous target for thermosensitive drug release. Furthermore, self-heating mitochondria-induced free radical blast could be an efficient therapeutic for deep-seated tumor therapy.

Why do nurses miss nursing care? A qualitative meta-synthesis.

AIM: The aim of this qualitative meta-synthesis was to discover the factors impacting on missed nursing care of nurses through systematic thinking. BACKGROUND: Although nurses are responsible for high-quality care, missed nursing care is common, endangering patient safety. Understanding of the causes related to missed nursing care could help nursing managers improve the quality of nursing care. DESIGN: A qualitative meta-synthesis guided by the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA). METHODS: As a method designed to contribute to knowledge development, meta-synthesis allows for integration of qualitative study findings using thematic synthesis. Six databases were searched up to October 2021; nine studies met the inclusion and quality assessment criteria and meta-synthesis were conducted. RESULTS: Three themes related to the causes why nurses missed nursing care were found. The themes included intrinsic resources (professional and ethical values, ambiguous nurse role, prioritization, education system, and knowledge), system structure (staff and resources shortage, heavy workload but limited time, and organizational management failure), and social environment (communication, working relationship and skill mix, and inappropriate ward layout). CONCLUSION: The phenomenon of missed nursing care is a global tissue, with variations in its elements but also notable similarities. Meta-synthesis provides evidence of intrinsic and extrinsic factors that contribute to missed nursing care. RELEVANCE TO CLINICAL PRACTICE: Recognizing and understanding the causes of missed nursing care is essential for nursing managers to ensure patient safety and the provision of high-quality care.

Farnesoid X receptor: From Structure to Function and Its Pharmacology in Liver Fibrosis.

The farnesoid X receptor (FXR), a ligand-activated transcription factor, plays a crucial role in regulating bile acid metabolism within the enterohepatic circulation. Beyond its involvement in metabolic disorders and immune imbalances affecting various tissues, FXR is implicated in microbiota modulation, gut- to-brain communication, and liver disease. The liver, as a pivotal metabolic and detoxification organ, is susceptible to damage from factors such as alcohol, viruses, drugs, and high-fat diets. Chronic or recurrent liver injury can culminate in liver fibrosis, which, if left untreated, may progress to cirrhosis and even liver cancer, posing significant health risks. However, therapeutic options for liver fibrosis remain limited in terms of FDA- approved drugs. Recent insights into the structure of FXR, coupled with animal and clinical investigations, have shed light on its potential pharmacological role in hepatic fibrosis. Progress has been achieved in both fundamental research and clinical applications. This review critically examines recent advancements in FXR research, highlighting challenges and potential mechanisms underlying its role in liver fibrosis treatment.

Calcium Tungstate Microgel Enhances the Delivery and Colonization of Probiotics during Colitis via Intestinal Ecological Niche Occupancy.

The effective delivery and colonization of probiotics are recommended for therapeutic interventions during colitis, the efficacy of which is hampered by abnormally colonized Enterobacteriaceae at pathological sites. To improve the delivery and colonization of probiotics, a calcium tungstate microgel (CTM)-based oral probiotic delivery system is proposed herein. CTM can selectively disrupt the ecological niche occupied by abnormally expanded Enterobacteriaceae during colitis to facilitate probiotic colonization. In addition, the calcium-binding protein, calprotectin, which is highly expressed in colitis, efficiently extracts calcium from CTM and releases tungsten to inhibit Enterobacteriaceae by displacing molybdenum in the molybdenum enzyme, without affecting the delivered probiotics. Moreover, CTM demonstrated resistance to the harsh environment of the gastrointestinal (GI) tract and to intestinal adhesion. The synergistic reduction of Enterobacteriaceae by 45 times and the increase in probiotic colonization by 25 times, therefore, result in a remarkable treatment for colitis, including restoration of colonic length, effective downregulation of the inflammatory response, restoration of the damaged mucosal barrier, and restoration of gut microbiome homeostasis.

Prediction of the mechanisms of action of Qutan Huoxue decoction in non-alcoholic steatohepatitis (NASH): a network pharmacology study and experimental validation.

CONTEXT: Qutan Huoxue decoction (QTHX) is used to treat non-alcoholic steatohepatitis (NASH) with good efficacy in the clinic. However, the mechanism is not clear yet. OBJECTIVE: This study investigates the mechanism of QTHX in the treatment of NASH. MATERIALS AND METHODS: Potential pathways of QTHX were predicted by network pharmacology. Fourty Sprague Dawley (SD) rats (half normal diet, half high-fat diet) were fed six to eight weeks, primary hepatocytes and Kupffer cells were extracted and co-cultured by the 0.4-micron trans well culture system. Then, the normal co-cultured cells were treated by normal serum, the NASH co-cultured cells were treated with various concentrations of QTHX-containing serum (0, 5, 7.5 or 10 µg/mL) for 24 h. The expression of targets were measured with Activity Fluorometric Assay, Western blot and PCR assay. RESULTS: Network pharmacology indicated that liver-protective effect of QTHX was associated with its anti-inflammation response, oxidative stress, and lipid receptor signalling. 10 µg/mL QTHX significantly reduced the inflammation response and lipid levels in primary hepatocytes (ALT: 46.43 ± 2.76 U/L, AST: 13.96 ± 1.08 U/L, TG: 0.25 ± 0.01 mmol/L, TC: 0.14 ± 0.05 mmol/L), comparing with 0 µg/mL NASH group (ALT: 148 ± 9.22 U/L, AST: 53.02 ± 2.30 U/L, TG: 0.74 ± 0.07 mmol/L, TC: 0.91 ± 0.07 mmol/L) (p < 0.01). Meanwhile, QTHX increased expression of SOCS1 and decreased expression of TLR4, Myd88, NF-κB. CONCLUSIONS: The study suggested that QTHX treats NASH in rats by activating the SCOS1/NF-κB/TLR4 pathway, suggesting QTHX could be further developed as a potential liver-protecting agent.

Nanodrug rescues liver fibrosis via synergistic therapy with H2O2 depletion and Saikosaponin b1 sustained release.

Hypoxia and hydrogen peroxide (H2O2) accumulation form the profibrogenic liver environment, which involves fibrogenesis and chronic stimulation of hepatic stellate cells (HSCs). Catalase (CAT) is the major antioxidant enzyme that catalyzes H2O2 into oxygen and water, which loses its activity in different liver diseases, especially in liver fibrosis. Clinical specimens of cirrhosis patients and liver fibrotic mice are collected in this work, and results show that CAT decrease is closely correlated with hypoxia-induced transforminmg growth factor ß1 (TGF-ß1). A multifunctional nanosystem combining CAT-like MnO2 and anti-fibrosis Saikosaponin b1 (Ssb1) is subsequently constructed for antifibrotic therapy. MnO2 catalyzes the accumulated H2O2 into oxygen, thereby ameliorating the hypoxic and oxidative stress to prevent activation of HSCs, and assists to enhance the antifibrotic pharmaceutical effect of Ssb1. This work suggests that TGF-ß1 is responsible for the diminished CAT in liver fibrosis, and our designed MnO2@PLGA/Ssb1 nanosystem displays enhanced antifibrotic efficiency through removing excess H2O2 and hypoxic stress, which may be a promising therapeutic approach for liver fibrosis treatment.

The pathogenesis of organ fibrosis: Focus on necroptosis.

Fibrosis is a common process of tissue repair response to multiple injuries in all chronic progressive diseases, which features with excessive deposition of extracellular matrix. Fibrosis can occur in all organs and tends to be nonreversible with the progress of the disease. Different cells types in different organs are involved in the occurrence and development of fibrosis, that is, hepatic stellate cells, pancreatic stellate cells, fibroblasts and myofibroblasts. Various types of programmed cell death, including apoptosis, autophagy, ferroptosis and necroptosis, are closely related to organ fibrosis. Among these programmed cell death types, necroptosis, an emerging regulated cell death type, is regarded as a huge potential target to ameliorate organ fibrosis. In this review, we summarize the role of necroptosis signalling in organ fibrosis and collate the small molecule compounds targeting necroptosis. In addition, we discuss the potential challenges, opportunities and open questions in using necroptosis signalling as a potential target for antifibrotic therapies. LINKED ARTICLES: This article is part of a themed issue on Translational Advances in Fibrosis as a Therapeutic Target. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v180.22/issuetoc.

From liver fibrosis to hepatocarcinogenesis: Role of excessive liver H2O2 and targeting nanotherapeutics.

Liver fibrosis and hepatocellular carcinoma (HCC) have been worldwide threats nowadays. Liver fibrosis is reversible in early stages but will develop precancerosis of HCC in cirrhotic stage. In pathological liver, excessive H2O2 is generated and accumulated, which impacts the functionality of hepatocytes, Kupffer cells (KCs) and hepatic stellate cells (HSCs), leading to genesis of fibrosis and HCC. H2O2 accumulation is associated with overproduction of superoxide anion (O2 •-) and abolished antioxidant enzyme systems. Plenty of therapeutics focused on H2O2 have shown satisfactory effects against liver fibrosis or HCC in different ways. This review summarized the reasons of liver H2O2 accumulation, and the role of H2O2 in genesis of liver fibrosis and HCC. Additionally, nanotherapeutics targeting H2O2 were summarized for further consideration of antifibrotic or antitumor therapy.

Identification of a novel ANK1 mutation in a Chinese family with hereditary spherocytosis: A case report.

The present study describes the clinical profile and ankyrin 1 (ANK1) mutation status of a Chinese family with hereditary spherocytosis (HS). A young male patient (proband) was diagnosed with HS after presenting with anaemia and jaundice. The Coombs test was negative and spherocytes were found in peripheral blood smears. Magnetic resonance imaging showed splenomegaly and splenic iron depositions. The red blood cell osmotic fragility test was positive. The eosin-5'-maleimide binding test showed reduced mean channel fluorescence. Whole-exome sequencing revealed a novel ANK1 mutation (c.4707G>A), resulting in a nonsense mutation (p.Trp1569*). The patient's father, paternal aunt and paternal grandmother exhibited comparable clinical symptoms and Sanger sequencing confirmed the same mutation in these family members. To the best of our knowledge, an HS pedigree with this novel ANK1 nonsense mutation has not been previously reported. At the same time, the unique clinical presentation of this pedigree helps our understanding of the heterogeneity of clinical manifestations of HS.

Moral distress, moral courage, and career identity among nurses: A cross-sectional study.

BACKGROUND: The concept of career identity is integral to nursing practices and forms the basis of the nursing professions. Positive career identity is essential for providing high-quality care, optimizing patient outcomes, and enhancing the retention of health professionals. Therefore, there is a need to explore potential influencing variables, thereby developing effective interventions to improve career identity. OBJECTIVES: To investigate the relationship between moral distress, moral courage, and career identity, and explore the mediating role of moral courage between moral distress and career identity among nurses. DESIGN: A quantitative, cross-sectional study. METHODS: A convenient sample of 800 nurses was recruited from two tertiary care hospitals between February and March 2022. Participants were assessed using the Moral Distress Scale-revised, Nurses' Moral Courage Scale, and Nursing Career Identity Scale. This study was described in accordance with the STROBE statement. ETHICAL CONSIDERATION: Research ethics approval was obtained from the researcher's university and hospital where this study was conducted prior to data collection. FINDINGS: Moral distress is negatively associated while moral courage is positively associated with career identity among nurses. Moral courage partially mediates the relationship between moral distress and career identity (ß = -0.230 to -0.163, p < 0.01). DISCUSSION: The findings reveal a relationship between moral distress, moral courage, and career identity among nurses. CONCLUSION: By paying attention to nurses' moral distress and courage, healthcare providers can contribute to the development of effective interventions to improve career identity, and subsequently performance, among nurses.

Integrated gut microbiota and serum metabolomics reveal the protective effect of oleanolic acid on liver and kidney-injured rats induced by Euphorbia pekinensis.

Euphorbia pekinensis (EP) is a commonly used Chinese medicine treating edema with potential hepatorenal toxicity. However, its toxic mechanism and prevention are remained to be explored. Oleanolic acid (OA) is a triterpene acid with potential hepatorenal protective activities. We investigated the protective effect and potential mechanism of OA on EP-induced hepatorenal toxicity. In this study, rats were given total diterpenes from EP (TDEP, 16 mg/kg) combined with OA (10, 20, 40 mg/kg) by gavage for 4 weeks. The results showed that TDEP administration could lead to a 3-4-fold increasement in hepatorenal biochemical parameters with histopathological injuries, while OA treatment could ameliorate them in a dose-dependent manner. At microbial and metabolic levels, intestinal flora and host metabolism were perturbed after TDEP administration. The disturbance of bile acid metabolism was the most significant metabolic pathway, with secondary bile acids increasing while conjugated bile acids decreased. OA treatment can improve the disorder of intestinal flora and metabolic bile acid spectrum. Further correlation analysis screened out that Escherichia-Shigella, Phascolarctobacterium, Acetatifactor, and Akkermansia were closely related to the bile acid metabolic disorder. In conclusion, oleanolic acid could prevent hepatorenal toxicity induced by EP by regulating bile acids metabolic disorder via intestinal flora improvement.

Bionic Regulators Break the Ecological Niche of Pathogenic Bacteria for Modulating Dysregulated Microbiome in Colitis.

Therapeutic approaches that reprogram the gut microbiome are promising strategies to alleviate and cure inflammatory bowel disease (IBD). However, abnormal expansion of Escherichia coli during inflammation can promote pathogenic bacteria occupying ecological niches to resist reprogramming of the microbiome. Herein, a bionic regulator (CaWO4 @YCW) is developed to efficiently and precisely regulate the gut microbiome by specifically suppressing the abnormal expansion of E. coli during colitis and boosting probiotic growth. Inspired by the binding of E. coli strains to the mannose-rich yeast cell wall (YCW), YCW is chosen as the bionic shell to encapsulate CaWO4 . It is demonstrated that the YCW shell endows CaWO4 with superior resistance to the harsh environment of the gastrointestinal tract and adheres to the abnormally expanded E. coli in colitis, specifically as a positioner. Notably, the high expression of calprotectin at the colitis site triggers the release of tungsten ions through calcium deprivation in CaWO4 , thus inhibiting E. coli growth by replacing molybdenum in the molybdopterin cofactor. Moreover, YCW functions as a prebiotic and promotes probiotic growth. Consequently, CaWO4 @YCW can efficiently and precisely reprogram the gut microbiome by eliminating pathogenic bacteria and providing prebiotics, resulting in an extraordinary therapeutic advantage for DSS-induced colitis.

Factors associated with failure of high-flow nasal cannula oxygen therapy in patients with severe COVID-19: a retrospective case series.

OBJECTIVE: To identify factors associated with high-flow nasal cannula (HFNC) therapy failure in patients with severe COVID-19. METHODS: We retrospectively examined clinical and laboratory data upon admission, treatments, and outcomes of patients with severe COVID-19. Sequential Organ Failure Assessment (SOFA) scores were also calculated. RESULTS: Of 54 patients with severe COVID-19, HFNC therapy was successful in 28 (51.9%) and unsuccessful in 26 (48.1%). HFNC therapy failure was more common in patients aged ≥60 years and in men. Compared with patients with successful HFNC therapy, patients with HFNC therapy failure had higher percentages of fatigue, anorexia, and cardiovascular disease; a longer time from symptom onset to diagnosis; higher SOFA scores; a higher body temperature, respiratory rate, and heart rate; more complications, including acute respiratory distress syndrome, septic shock, myocardial damage, and acute kidney injury; a higher C-reactive protein concentration, neutrophil count, and prothrombin time; and a lower arterial partial pressure of oxygen/fraction of inspired oxygen (PaO2/FiO2). However, male sex, a low PaO2/FiO2, and a high SOFA score were the only independent factors significantly associated with HFNC therapy failure. CONCLUSIONS: Male sex, a low PaO2/FiO2, and a high SOFA score were independently associated with HFNC therapy failure in patients with severe COVID-19.

Physiologically Inspired Mucin Coated Escherichia coli Nissle 1917 Enhances Biotherapy by Regulating the Pathological Microenvironment to Improve Intestinal Colonization.

The delivery of probiotics to the microbiota is a promising method to prevent and treat diseases. However, oral probiotics will suffer from gastrointestinal insults, especially the pathological microenvironment of inflammatory diseases such as reactive oxygen species (ROS) and the exhausted mucus layer, which can limit their survival and colonization in the intestinal tract. Inspired by the fact that probiotics colonized and grew in the mucus layer under physiological conditions, we developed a strategy for a super probiotic (EcN@TA-Ca2+@Mucin) coated with tannic acid and mucin via layer-by-layer technology. We demonstrated that mucin endows probiotics with superior resistance to the harsh environment of the gastrointestinal tract and with strong adhesiveness to the intestine through its interaction with mucus, which enhanced colonization and growth of probiotics in the mucus layer without removing the coating. Moreover, EcN@TA-Ca2+@Mucin can distinctly down-regulate inflammation with ROS scavenging and reduce the side effects of bacterial translocation in inflammatory bowel diseases, increasing the abundance and diversity of the gut microflora. We envision that it is a powerful platform to improve the colonization of probiotics by regulating the pathological microenvironment, which is expected to provide an important perspective for applying the intestinal colonization of probiotics to treat a variety of diseases.

Targeting Sirtuin1 to treat aging-related tissue fibrosis: From prevention to therapy.

Fibrosis, which is characterized by excessive extracellular matrix (ECM) deposition, is a wound-healing response to organ injury and may promote cancer and failure in various organs, such as the heart, liver, lung, and kidney. Aging associated with oxidative stress and inflammation exacerbates cellular dysfunction, tissue failure, and body function disorders, all of which are closely related to fibrosis. Sirtuin-1 (SIRT1) is a class III histone deacetylase that regulates growth, transcription, aging, and metabolism in various organs. This protein is downregulated in organ injury and fibrosis associated with aging. Its expression and distribution change with age in different organs and play critical roles in tissue oxidative stress and inflammation. This review first described the background on fibrosis and regulatory functions of SIRT1. Second, we summarized the relationships of SIRT1 with other proteins and its protective action during fibrosis in the heart, liver, lung and kidney. Third, the activation of SIRT1 in therapies of tissue fibrosis, especially in liver fibrosis and aging-related tissue injury, was analyzed. In conclusion, SIRT1 targeting may be a new therapeutic strategy in fibrosis.

Free radicals for cancer theranostics.

Free radicals were generally regarded as highly reactive, transient and harmful species. In fact, some of the free radicals can also be inactive, long-lived and beneficial for our health. These properties of free radicals provide future possibilities for their application in various fields. Owning to their open-shell electronic structure, free radicals exhibit unique advantages in biomedical applications, such as high reactivity, photoacoustic and photothermal conversion ability, molecular magnetic. In this review, recent progress on free radicals and their applications in cancer theranostics are presented. Typical materials that exhibit controlled generation of free radicals and their applications for photodynamic therapy (PDT), chemodynamic therapy (CDT), sonodynamic therapy (SDT), gas therapy, hypoxic cancer treatment, photothermal therapy (PTT), photoacoustic imaging (PAI) and magnetic resonance imaging (MRI) are summarized and discussed.

Effects of Qutan Huoxue Formula on the SOCS1/TLR4 Signaling Pathway in NASH Model Mice.

The purpose of this study was to investigate the effects of Qutan Huoxue Formula (QHF) on liver injury in mice with nonalcoholic steatohepatitis (NASH) by upregulating SOCS1 to inhibit the TLR4/NF-κB signaling pathway. Thirty male C57BL/6J mice (20-22 g) were randomly divided into the normal diet group (ND group), methionine- and choline-deficient diet group (MCD group), and Qutan Huoxue Formula group (QHF group). Mice in the ND group were fed a regular diet, while mice in other two groups were fed MCD diet. After successful molding, the QHF group was gavaged by QHF. The ND group and MCD group were gavaged by the same volume of normal saline, once a day. During the period of gavaging, all mice continue to be fed MCD fodder except for the ND group. All mice were killed at 8 w. H&E staining and Oil Red O staining were used to observe the pathological changes of liver tissues. Serum level of ALT, AST, TC, and TG was detected by enzyme-linked immunosorbent assay. The expression of liver SOCS1, TLR4, Myd88, and NF-κB was detected by real-time PCR, immunohistochemistry, and Western blot. QHF can significantly reduce the serum levels of ALT, AST, TC, and TG of NASH mice and reduce the degree of liver fat degeneration and inflammation. It also can decrease both mRNA and protein expressions of liver TLR4, Myd88, and NF-κB. The mRNA expression of SOCS1 increased, while the SOCS1 protein expression decreased. In conclusion, QHF can significantly alleviate hepatic steatosis and inflammation in NASH mice by upregulating SOCS1 to inhibit the TLR4/NF-κB signaling pathway.

Effects of Qutanhuoxue Decoction on AQP7 and AQP9 Expression in Nonalcoholic Fatty Liver Model Rats.

The purpose of this study was to investigate the effect of Qutanhuoxue decoction on AQP7 and AQP9 expression in nonalcoholic fatty liver model rats. Nighty male SD rats (six weeks old, 250 ± 10 g) were randomly divided into 5 groups: normal diet group (ND group), high-fat diet (HFD group), HFD + low dose Qd group, HFD + middle dose Qd group, and HFD + high dose Qd group. Rats in ND group were fed with a regular diet, while rats in other groups were fed with high-fat diet. After the success of the molding, HFD + low dose Qd group, HFD + middle dose Qd group, and HFD + high dose Qd group were, respectively, gavaged by Qutanhuoxue decoction with concentration of 4.5g.kg-1.d-1, 9.0g.kg-1.d-1, and 18g.kg-1.d-1. The ND group and HFD group were gavaged by the same volume of physiological saline lavage, once a day. During the period of gavaging, the other four groups continue to be fed with high-fat fodder except ND group. All rats were killed at 14d, 21d, and 28d, respectively. HE staining was used to observe the pathological changes of liver tissues and serum level of ALT AST GGT and TC TG was detected by automatic analyzer. The expression levels of liver AQP9 mRNA and adipose tissue AQP7 mRNA were detected by real-time PCR. Quhuoxue decoction can significantly reduce the liver function (ALT, AST, and GGT) and blood fat (TG, TC) levels of NAFLD rats and reduce the degree of liver fat degeneration. The effect was the best in the HFD + high dose Qd group of 28d. Qutanhuoxue decoction can decrease the expression of liver AQP9 mRNA and increase the expression of adipose tissue AQP7 mRNA. In conclusion, Qutanhuoxue decoction can reduce the degree of hepatic steatosis, which may be closely related to the increase of AQP7 expression in adipose tissue and the decrease of AQP9 expression in liver.