scholarly journals Hypertriglyceridemia and obesity exacerbate the course of SIRS induced by SAP in Rats

2019 ◽  
Author(s):  
Kelei Hua ◽  
RuiXia Li ◽  
LiYing Cao ◽  
WanSheng Lao
Keyword(s):  
Early Stage ◽  
Sodium Taurocholate ◽  
Serum Levels ◽  
Underlying Mechanism ◽  
Pancreatic Injury ◽  
Interleukin 10 ◽  
Histological Evaluation ◽  
Necrosis Factor Alpha ◽  
Blood Calcium ◽  
Tnf Α

AbstractThe aim of the present study was to explore the mechanism underlying how HTG (hypertriglyceridaemia) and obesity exacerbate the course of the systemic inflammatory response syndrome (SIRS) induced by severe acute pancreatitis (SAP) in rats. Seventy-two rats were fed a normal or high-fat diet to induce HTG and obesity, and SAP was induced by retrograde injection of 5% sodium taurocholate solution at a volume of 1 ml/kg into the biliopancreatic duct. The injury to the pancreas was assessed by macroscopic observation, pancreatic histological evaluation and serum levels of amylase and lipase. SIRS was estimated by measuring SIRS scores and interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-α) and interleukin-10 (IL-10) expression. The results showed that the SIRS scores and pancreatic histological scores increased significantly and the blood calcium level decreased significantly in the hypertriglyceridaemia SAP (HSAP) group compared with those of the SAP group. In addition, HTG and obesity significantly increased plasma levels of the proinflammatory cytokines IL-6 and TNF-α and significantly downregulated the proinflammatory cytokine IL-10. Our findings showed that HSAP rats exhibited more severe pancreatic injury and more serious SIRS scores than the SAP rats did. The underlying mechanism may be that HTG and obesity intensify early-stage SIRS by regulating the levels of inflammatory and anti-inflammatory cytokines.

scholarly journals Adenovirus-mediated artificial miRNA targetting fibrinogen-like protein 2 attenuates the severity of acute pancreatitis in mice

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Xiaohua Ye ◽  
Jin Ding ◽  
Yanping Chen ◽  
Jiayue Dong
Keyword(s):  
Acute Pancreatitis ◽  
Western Blotting ◽  
Early Stage ◽  
Sodium Taurocholate ◽  
Pancreatic Injury ◽  
Protective Role ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Mrna Levels ◽  
Artificial Mirna ◽  
Tnf Α

Severe acute pancreatitis (SAP) remains to be challenging for its unpredictable inflammatory progression from acute pancreatitis to SAP. Apoptosis is an important pathology of SAP. Fibrinogen-like protein 2 (FGL2) has been reported to be involved in apoptosis. The present study aimed to explore the therapeutic effect of an adenovirus-mediated artificial miRNA targetting FGL2 (Ad-FGL2-miRNA) in taurocholate-induced murine pancreatitis models. Sodium taurocholate was retrogradely injected into the biliopancreatic ducts of the C57/BL mice to induce SAP. FGL2 expression was measured with reverse transcription-PCR, Western blotting, and immunohistochemical staining. ELISA was used to detect the activity of amylase and the concentrations of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). In addition, the mRNA levels of TNF-α and IL-1β were also detected. Finally, apoptosis was assessed by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeling (TUNEL) method and Western blotting. Ad-FGL2-miRNA significantly suppressed FGL2 expression and alleviated pancreatic injury. Also, Ad-FGL2-miRNA markedly inhibited a post-SAP increase in the activation of TNF-α and IL-1β. Finally, pretreatment with Ad-FGL2-miRNA ameliorated apoptosis at the early stage of SAP by modulating cleaved caspase-3 and therefore played a protective role. These results indicated that FGL2 might be a promising target for attenuating the severity of SAP and adenovirus-mediated artificial miRNAs targetting FGL2 represented a potential therapeutic approach for the treatment of SAP.

scholarly journals Interleukin-10 Controls the Onset of Irreversible Septic Shock

2002 ◽  
Vol 70 (8) ◽  
pp. 4441-4446 ◽  
Author(s):  
Samir Q. Latifi ◽  
Mary Ann O'Riordan ◽  
Alan D. Levine
Keyword(s):  
Septic Shock ◽  
Interleukin 1 ◽  
Late Phase ◽  
Cecal Ligation ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Therapeutic Window ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cytokine Cascade

ABSTRACT Lethality from sepsis is believed to be mediated by a proinflammatory cytokine cascade, yet blocking the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) fails to prevent mortality in human disease and a mouse model of sepsis induced by cecal ligation and puncture (CLP). The role of the antiinflammatory cytokine IL-10 in the CLP model of sepsis is unclear, with either protective or harmful effects demonstrated, depending upon the time of intervention. We therefore hypothesize that IL-10 functions as a temporal regulator of the transition from early reversible sepsis to the late phase of irreversible shock. Transition from reversible sepsis to irreversible shock in the CLP model was defined as the time when removal of the necrotic cecum by rescue surgery is no longer effective. We subjected IL-10-deficient (IL-10−/−) and wild-type (IL-10+/+) mice to CLP and monitored the progression of sepsis, the onset of irreversible shock, and mortality. Onset of lethality in IL-10−/− mice occurred significantly earlier than in IL-10+/+ mice and was associated with 15-fold-higher serum levels of TNF-α and IL-6. Consistent with these findings, the efficacy of rescue surgery after lethal CLP is lost 10 h earlier in IL-10−/− mice than in IL-10+/+ mice. Treatment with recombinant human IL-10 5 h after CLP significantly improved survival and lengthened the therapeutic window for rescue surgery in both strains of mice. These results demonstrate that IL-10 controls the onset of irreversible septic shock after CLP.

Higher Interleukin-10 (IL-10) and Lower Interferon-Gamma (IFN-γ), Tumor Necrosis Factor Alpha (TNF-α), IL-6, IL-8 Serum Levels in Patients Undergoing Reduced Intensity Versus Conventional Intensity Conditioning Hematopoietic Cell Transplantation (HCT).

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 5208-5208
Author(s):  
H. Stradmann ◽  
Ute Hegenbart ◽  
M. Bruegel ◽  
Haifa K. Al-Ali ◽  
Dietger W. Niederwieser
Keyword(s):  
Hematopoietic Cell Transplantation ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
Allogeneic Hct ◽  
Hematopoietic Reconstitution ◽  
Tnf Α ◽  
Ifn Γ ◽  
Reduced Intensity ◽  
Related Mortality

Abstract Endogenous cytokines play an essential role in allogeneic HCT not only for hematopoietic reconstitution but also for the most frequent complications of HCT such as graft-versus-host disease (GvHD). Cytokines have important immune modulatory effects and are therefore important determinants for outcome. No report, however, exists to date on the role of cytokines in HCT with reduced intensity conditioning (RIC), which are associated with less severe GVHD and reduced transplant related mortality. Patients transplanted at the University of Leipzig between October 2000 and November 2001 with an autologous (n=10) or allogeneic (n=38) related or unrelated graft were included in this analysis. The median age of patients was 49 (range 21–69) years. Preparative regimens for the allogeneic HCT consisted of conventional (n=20) or RIC (n=18) conditioning. Cyclophosphamide (60mg/kg for 2 consecutive days) was given either with busulfan (4 mg/kg per day for 4 days; n=9) or fractioned total body irradiation (TBI 12 Gy; n=11) for conventional HCT and cyclosporine in combination with metotrexate was used as GvHD prophylaxis. In contrast, patients with the reduced intensity treatment received low dose TBI (2 Gy) in combination with fludarabine (30 mg/m2 per day for 3 consecutive days) followed by cyclosporine and mycophenolat mofetil. Serum was collected three times weekly and was frozen at −70° until measurement. Cytokine-serum-levels were analyzed with a Multiplex Cytokine Assay (Bio-Plex, Bio-Rad Laboratories, Hercules, CA). Endogenous IFN-γ and TNF-α showed similar fluctuations after RIC and non-RIC HCT with peak levels between day 14/17. However, serum levels of non-RIC patients increased faster than serum levels of RIC-patients. Higher IL-4 serum levels were detected in the RIC patients as compared to the non-RIC patients especially in the later course of HCT. In contrast, higher IL-6 and IL-8 values with peaks at d 6/9 in both groups were observed in the patients with conventional HCT. Similarly a difference for IL-13 levels was detected with higher values for the conventional group. The most prominent difference was observed in the endogenous IL-10 production with significant higher IL-10 levels in RIC compared to non-RIC patients. We concluded that serum levels of IL-4 and IL-10 were higher and IFN-γ, TNF-α, IL-6, IL-8 and IL-13 lower in the RIC compared to the non-RIC group. These results are in line with previous work on cytokines after conventional preparative regimen and might provide an explanation for the lower transplant related mortality of RIC regimens.

Alterations of serum levels of plasminogen, TNF-α, and IDO in granulomatosis with polyangiitis patients

Vascular ◽  
2021 ◽  
pp. 170853812098630
Author(s):  
Dobroslav Kyurkchiev ◽  
Tsvetelina Yoneva ◽  
Adelina Yordanova ◽  
Ekaterina Kurteva ◽  
Georgi Vasilev ◽  
...  
Keyword(s):  
Granulomatosis With Polyangiitis ◽  
Renal Involvement ◽  
Clinical Manifestations ◽  
Area Under The Curve ◽  
Serum Levels ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Spearman's Rho ◽  
Tnf Α ◽  
Spearman’S Rho

Background Granulomatosis with polyangiitis (GPA) is a representative of vasculitides associated with anti-neutrophil cytoplasmic autoantibodies. “Classical” antibodies directed against proteinase 3 are involved in the pathogenesis and are part of the GPA diagnosis at the same time. Along with them, however, antibodies against Lysosomal-Associated Membrane Protein-2 (LAMP-2) and antibodies directed against plasminogen have been described in GPA. Objectives and methodology: We performed a cross-sectional study enrolling 34 patients diagnosed with GPA. Our study was aimed at looking for correlations between serum levels of LAMP-2 and plasminogen and the clinical manifestations of the GPA. Furthermore, we examined serum levels of tumor necrosis factor-alpha (TNF-α) and its associated indoleamine-pyrrole 2,3-dioxygenase (IDO), as well as we looked for a correlation between these cytokines and the clinical manifestations of GPA. Results The results showed that in GPA, serum plasminogen levels were negatively associated with renal involvement (receiver operating characteristic (ROC) area under the curve (AUC) of 0.78) (95% CI 0.53–0.91), p = 0.035, and the extent of proteinuria, Spearman’s Rho = –0.4, p = 0.015. Increased levels of TNF-α and IDO correlated with disease activity, Spearman’s Rho =0.62, p = 0.001 and Spearman’s Rho = 0.4, p = 0.022, respectively, whereas only TNF-α was increased in severe forms of GPA with lung involvement (ROC AUC of 0.8) (95% CI 0.66–0.94), p = 0.005. Conclusions In this study, we demonstrate the alteration of soluble factors, which play an important role in the pathogenesis of GPA and their relationship with the clinical manifestations of the disease. Our main results confirm the associations of increased secretory TNF-α and some clinical manifestations, and we describe for the first time decreased serum plasminogen levels and their association with renal involvement.

scholarly journals Trehalose 6,6′-Dimycolate (Cord Factor) of Mycobacterium tuberculosis Induces Corneal Angiogenesis in Rats

2000 ◽  
Vol 68 (10) ◽  
pp. 5991-5997 ◽  
Author(s):  
Norio Saita ◽  
Nagatoshi Fujiwara ◽  
Ikuya Yano ◽  
Kazuhiko Soejima ◽  
Kazuo Kobayashi
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Neutralizing Antibodies ◽  
Early Stage ◽  
Vascular Endothelial ◽  
Cytokine Network ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cord Factor ◽  
Factor Alpha ◽  
Endothelial Growth Factor

ABSTRACT Neovascularization or angiogenesis is required for the progression of chronic inflammation. The mechanism of inflammatory neovascularization in tuberculosis remains unknown. Trehalose 6,6′-dimycolate (TDM) purified from Mycobacterium tuberculosis was injected into rat corneas. TDM challenge provoked a local granulomatous response in association with neovascularization. Neovascularization was seen within a few days after the challenge, with the extent of neovascularization being dose dependent, although granulomatous lesions developed 14 days after the challenge. Cytokines, including tumor necrosis factor alpha (TNF-α), interleukin-8 (IL-8), IL-1β, and vascular endothelial growth factor (VEGF), were found in lesions at the early stage (within a few days after the challenge) and were detectable until day 21. Neovascularization was inhibited substantially by neutralizing antibodies to VEGF and IL-8 but not IL-1β. Treatment with anti-TNF-α antibodies resulted in partial inhibition. TDM possesses pleiotropic activities, and the cytokine network plays an important role in the process of neovascularization.

scholarly journals Protective effects of Panax notoginseng saponins in a rat model of severe acute pancreatitis occur through regulation of inflammatory pathway signaling by upregulation of miR-181b

2018 ◽  
Vol 32 ◽  
pp. 205873841881863
Author(s):  
Ming-wei Liu ◽  
Yun-qiao Huang ◽  
Ya-ping Qu ◽  
Dong-mei Wang ◽  
Deng-yun Tang ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Rat Model ◽  
Therapeutic Potential ◽  
Sodium Taurocholate ◽  
Panax Notoginseng ◽  
Serum Levels ◽  
Panax Notoginseng Saponins ◽  
Tnf Α ◽  
Anti Inflammatory

Panax notoginseng saponins are extracted from Chinese ginseng— Panax notoginseng Ledeb—and are known to have therapeutic anti-inflammatory effects. However, the precise mechanism behind their anti-inflammatory effects remains relatively unknown. To better understand how Panax notoginseng saponins exert their therapeutic benefit, we tested them in a rat model of severe acute pancreatitis (SAP). Rats received a tail vein injection of Panax notoginseng saponins and were administered 5% sodium taurocholate 2 h later. Pancreatic tissue was then harvested and levels of miR-181b, FSTL1, TREM1, TLR4, TRAF6, IRAK1, p-Akt, p-p38MAPK, NF-κBp65, and p-IκB-α were determined using Western blot and quantitative real-time polymerase chain reaction (qRT-PCR). Enzyme-linked immunosorbent assays were used to determine serum levels of tumor necrosis factor-α (TNF-α), TREM1, interleukin (IL)-6, ACAM-1, IL-8, and IL-12 and DNA-bound levels of NF-KB65 and TLR4 in pancreatic and ileum tissue. Serum levels of lipase and amylase, pancreatic myeloperoxidase (MPO) activity, and pancreatic water content were also measured. Hematoxylin and eosin staining was used for all histological analyses. Results indicated upregulation of miR-181b, but negligible levels of FSTL1, p-p38MAPK, TLR4, TRAF6, p-Akt, IRAK1, TREM1, p-NF-κBp65, and p-IκB-α, as well as negligible DNA-bound levels of NF-KB65 and TLR4. We also observed lower levels of IL-8, IL-6, ACAM-1, TNF-α, MPO, and IL-12 in the Panax notoginseng saponin–treated group when compared with controls. In addition, Panax notoginseng saponin–treated rats had significantly reduced serum levels of lipase and amylase. Histological analyses confirmed that Panax notoginseng saponin treatment significantly reduced taurocholate-induced pancreatic inflammation. Collectively, our results suggest that Panax notoginseng saponin treatment attenuated acute pancreatitis and pancreatic inflammation by increasing miR-181b signaling. These findings suggest that Panax notoginseng saponins have therapeutic potential in the treatment of taurocholate-induced SAP.

scholarly journals Type 17 Immune Response Facilitates Progression of Inflammation and Correlates with Cognition in Stable Schizophrenia

Diagnostics ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 926
Author(s):  
Milica M. Borovcanin ◽  
Slavica Minic Janicijevic ◽  
Ivan P. Jovanovic ◽  
Nevena M. Gajovic ◽  
Milena M. Jurisevic ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Peripheral Blood ◽  
Cd4 T Cells ◽  
Serum Levels ◽  
Antipsychotic Therapy ◽  
Necrosis Factor Alpha ◽  
Positive Correlation ◽  
Tnf Α ◽  
Immune Pathway

Dysregulation of the type 17 immune pathway has already been considered in schizophrenia and we previously measured decreased sera values of interleukin (IL)-17 in early stages. We further explored the possible correlation of IL-17 systemic levels with proinflammatory cytokines and cognitive scores and additionally analyzed the percentage of IL-17 producing lymphocytes in peripheral blood of patients with stable schizophrenia. We included 27 patients diagnosed with schizophrenia (F20), after a three-month stable depot antipsychotic therapy (risperidone or paliperidone) and 18 healthy control subjects. Positive and Negative Syndrome Scale of Schizophrenia and the Montreal-Cognitive Assessment (MoCA) were conducted. Sera concentrations of IL-17, IL-6, tumor necrosis factor alpha (TNF-α) and soluble ST2 receptor (sST2) were measured. Flow cytometry and Natural Killer (NK) and T cell analyses were done in 10 patients and 10 healthy controls. Moderate positive correlation was established between IL-17 and TNF-α (r = 0.640; p = 0.001), IL-17 and IL-6 (r = 0.514; p = 0.006), IL-17 and sST2 (r = 0.394; p = 0.042). Furthermore, a positive correlation between the serum levels of IL-17 and MoCA scores was observed, especially with visuospatial and executive functioning, as well as language functioning and delayed recall (p < 0.05). Significantly higher percentage of IL-17 producing CD56+ NK cells was measured in peripheral blood of patients with schizophrenia in remission vs. healthy individuals (p = 0.001). The percentage of CD4+ T cells and CD4+ T cells that produce IL-17 was significantly increased in patients (p = 0.001). This study revealed the involvement of innate type 17 immune response in the progression of inflammation and this could be related to cognitive functioning in stable schizophrenia.

scholarly journals A Defect in Interleukin-10 Leads to Enhanced Malarial Disease in Plasmodium chabaudi chabaudi Infection in Mice

1999 ◽  
Vol 67 (9) ◽  
pp. 4435-4442 ◽  
Author(s):  
Ching Li ◽  
Inés Corraliza ◽  
Jean Langhorne
Keyword(s):  
Body Weight ◽  
Knockout Mice ◽  
Interleukin 10 ◽  
Plasmodium Chabaudi ◽  
Double Knockout ◽  
Direct Stimulation ◽  
Necrosis Factor Alpha ◽  
Glucose Levels ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACT Infection of interleukin-10 (IL-10)-nonexpressing (IL-10−/−) mice with Plasmodium chabaudi chabaudi (AS) leads to exacerbated pathology in female mice and death in a proportion of them. Hypoglycemia, hypothermia, and loss in body weight were significantly greater in female IL-10−/−mice than in male knockout mice and all wild-type (WT) mice during the acute phase of infection. At this time, both female and male IL-10−/− mice produced more gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), and IL-12p40 mRNA than their respective WT counterparts. Inactivation of IFN-γ in IL-10−/− mice by the injection of anti-IFN-γ antibodies or by the generation of IL-10−/− IFN-γ receptor−/− double-knockout mice resulted in reduced mortality but did not affect body weight, temperature, or blood glucose levels. The data suggest that IFN-γ-independent pathways may be responsible for these pathological features of P. chabaudimalaria and may be due to direct stimulation of TNF-α by the parasite. Since male and female knockout mice both produce more inflammatory cytokines than their WT counterparts, it is likely that the mortality seen in females is due to the nature or magnitude of the response to these cytokines rather than the amount of IFN-γ or TNF-α produced.

scholarly journals The Host Antimicrobial Protein Calgranulin C Participates in the Control ofCampylobacter jejuniGrowth via Zinc Sequestration

2018 ◽  
Vol 86 (6) ◽  
Author(s):  
Janette M. Shank ◽  
Brittni R. Kelley ◽  
Joseph W. Jackson ◽  
Jessica L. Tweedie ◽  
Dana Franklin ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Poultry Meat ◽  
Antimicrobial Protein ◽  
Dependent Manner ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Full Resolution ◽  
Factor Alpha

ABSTRACTCampylobacter jejuniis a leading cause of bacterially derived gastroenteritis worldwide.Campylobacteris most commonly acquired through the consumption of undercooked poultry meat or through drinking contaminated water. Following ingestion,Campylobacteradheres to the intestinal epithelium and mucus layer, causing toxin-mediated inflammation and inhibition of fluid reabsorption. Currently, the human response to infection is relatively unknown, and animal hosts that model these responses are rare. As such, we examined patient fecal samples for the accumulation of the neutrophil protein calgranulin C during infection withCampylobacter jejuni. In response to infection, calgranulin C was significantly increased in the feces of humans. To determine whether calgranulin C accumulation occurs in an animal model, we examined disease in ferrets. Ferrets were effectively infected byC. jejuni, with peak fecal loads observed at day 3 postinfection and full resolution by day 12. Serum levels of interleukin-10 (IL-10) and tumor necrosis factor alpha (TNF-α) significantly increased in response to infection, which resulted in leukocyte trafficking to the colon. As a result, calgranulin C increased in the feces of ferrets at the time whenC. jejuniloads decreased. Further, the addition of purified calgranulin C toC. jejunicultures was found to inhibit growth in a zinc-dependent manner. These results suggest that upon infection withC. jejuni, leukocytes trafficked to the intestine release calgranulin C as a mechanism for inhibitingC. jejunigrowth.

scholarly journals Effects of Shugan-Jianpi Recipe on the Expression of the p38 MAPK/NF-κB Signaling Pathway in the Hepatocytes of NAFLD Rats

Medicines ◽  
2018 ◽  
Vol 5 (3) ◽  
pp. 106 ◽  
Author(s):  
Yuanjun Deng ◽  
Kairui Tang ◽  
Runsen Chen ◽  
Yajie Liu ◽  
Huan Nie ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
Low Dose ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
High Dose ◽  
Model Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Background: In traditional Chinese medicine, the Shugan-Jianpi recipe is often used in the treatment of nonalcoholic fatty liver disease (NAFLD). This study aimed to explore the mechanism of the Shugan-Jianpi recipe in relation to rats with NAFLD induced by a high-fat diet. Methods: Rats were randomly divided into eight groups: normal group (NG), model group (MG), low-dose Chaihu–Shugan–San group (L-CG), high-dose Chaihu–Shugan–San group (H-CG), low-dose Shenling–Baizhu–San group (L-SG), high-dose Shenling–Baizhu–San group (H-SG), low dose of integrated-recipes group (L-IG), and high dose of integrated-recipes group (H-IG). After 26 weeks, a lipid profile, aspartate, and alanine aminotransferases in serum were detected. The serum levels of inflammatory factors including interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were analyzed using the enzyme linked immunosorbent assay (ELISA) method. Hepatic pathological changes were observed with hematoxylin-eosin (HE) and oil red O staining. The expression of the p38 mitogen-activated protein kinases (MAPK)/nuclear factor-κB (NF-κB) pathway was detected by quantitative real-time PCR and Western blotting. Results: A pathological section revealed that NAFLD rats have been successfully reproduced. Compared with the model group, each treatment group had different degrees of improvement. The Shugan-Jianpi recipe can inhibit the serum levels of IL-1β, IL-6, and TNF-α in NAFLD rats. The expression of mRNA and a protein related to the p38 MAPK/NF-κB signaling pathway were markedly decreased as a result of the Shugan-Jianpi recipe. Conclusions: The Shugan-Jianpi recipe could attenuate NAFLD progression, and its mechanism may be related to the suppression of the p38 MAPK/NF-κB signaling pathway in hepatocytes.

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