scholarly journals Effect of dexamethasone on levels of inflammatory factors and EGF mRNA in rabbits suffering from oral ulcers

2022 ◽  
Vol 20 (2) ◽  
pp. 351-357
Author(s):  
Weiliang Wu ◽  
Jianyong Ruan ◽  
Daxu Li ◽  
Hong Tao ◽  
Chunni Deng ◽  
...  
Keyword(s):  
Acetic Acid Solution ◽  
Rabbit Model ◽  
Inflammatory Cells ◽  
Underlying Mechanism ◽  
Oral Ulcer ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Oral Ulcers ◽  
Tnf Α ◽  
Group B

Purpose: To investigate the therapeutic effect of dexamethasone on rabbits suffering from oral ulcers, and the underlying mechanism(s) of action. Methods: A rabbit model of oral ulcer was established by applying 40 % glacial acetic acid solution to the oral buccal membranes of the animals. Three groups of rabbits were used. Changes in area of the oral ulcer were recorded after dexamethasone administration. Levels of epidermal growth factor (EGF) were assayed using reverse transcription PCR (RT-PCR), while MDA levels and expression levels of IL- 6, IL-8 and TNF-α were determined by enzyme-linked immunosorbent assay (ELISA). Local histopathological changes were examined histologically with the aid of hematoxylin and eosin (H & E) staining. Results: There were reductions in ulcer areas in group C on the 2nd, 4th and 7th days of dexamethasone administration, when compared with group B (p < 0.05). The EGF levels in the buccal mucosa of rabbits in groups B and C were significantly higher than those in group A (p < 0.05), while the highest EGF level was in group C (p < 0.05). The levels of MDA, IL-6, IL-8, and TNF-α significantly increased in groups B and C (p < 0.05). Results from H & E staining showed lower levels of inflammatory cells in group C than in group B, with visible proliferation of fibroblast cells and epithelial cells in group C after dexamethasone administration. Conclusion: Dexamethasone accelerates healing of oral ulcer by regulating EGF levels. This finding provides a new approach to the treatment of oral ulcers.

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.

scholarly journals Plasma BDNF and Cytokines Correlated with Protein Biomarkers for Bipolar II Disorder

2021 ◽  
Vol 11 (12) ◽  
pp. 1282
Author(s):  
Sheng-Yu Lee ◽  
Tzu-Yun Wang ◽  
Ru-Band Lu ◽  
Liang-Jen Wang ◽  
Cheng-Ho Chang ◽  
...  
Keyword(s):  
Underlying Mechanism ◽  
Trna Synthetase ◽  
Inflammatory Factors ◽  
Control Group ◽  
Protein Biomarkers ◽  
Bdnf Level ◽  
Bipolar Ii Disorder ◽  
Bipolar Ii ◽  
Tnf Α ◽  
Factor Α

We have previously identified five candidate proteins (matrix metallopeptidase 9 (MMP9), phenylalanyl-TRNA synthetase subunit beta (FARSB), peroxiredoxin 2 (PRDX2), carbonic anhydrase 1 (CA-1), and proprotein convertase subtilisin/kexin Type 9 (PCSK9)) as potential biomarkers for bipolar II disorder (BD-II). These candidate proteins have been associated with neuroprotective factors (BDNF) and inflammatory factors (cytokines, C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α)). However, the correlations between these proteins with plasma BDNF and inflammatory factors remain unknown. We recruited a total of 185 patients with BD-II and 186 healthy controls. Plasma levels of candidate proteins, BDNF, cytokines (TNF-α, CRP, and interleukin-8 (IL-8)) were assessed from each participant. The correlations between levels of candidate proteins, BDNF, and cytokines were analyzed. In the BD-II group, we found that the level of FARSB was positively correlated with the BDNF level (r = 0.397, p < 0.001) and IL-8 (r = 0.320, p < 0.001). The CA-1 level positively correlated with IL-8 (r = 0.318, p < 0.001). In the control group, we found that the FARSB level positively correlated with the BDNF level (r = 0.648, p < 0.001). The CA-1 level positively correlated with TNF-α (r = 0.231, p = 0.002), while the MMP-9 level positively correlated with the CRP level (r = 0.227, p = 0.002). Our results may help in clarifying the underlying mechanism of these candidate proteins for BD-II.

scholarly journals Floroindole confers protection against cecal ligation and puncture-induced sepsis via inhibition of NF-kB p65 phosphorylation

2021 ◽  
Vol 18 (6) ◽  
pp. 1161-1166
Author(s):  
Zhiwen Zhou ◽  
Xiang Ren ◽  
Aiping Li ◽  
Wensheng Zhou ◽  
Li Huang
Keyword(s):  
Quantitative Polymerase Chain Reaction ◽  
Cecal Ligation ◽  
Underlying Mechanism ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Cecal Ligation And Puncture ◽  
Degree Of Protection ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Factor Α

Purpose: To investigate the protective effect of floroindole against cecal ligation and puncture (CLP)- induced sepsis, as well as the underlying mechanism of action. Methods: Thirty-five 10–week-old male Wistar rats weighing 190 - 210 g (mean: 200.00 ± 10.10 g) were used for this study. The rats were randomly assigned to seven groups of five rats each, viz, normal control group, and six CLP groups. The CLP groups were those subjected to cecal ligation and puncture (CLP). The first 5 CLP groups received 2, 4, 6, 8 or 10 mg/kg floroindole, respectively, 1 h after CLP, via intraperitoneal route (i.p.) while the 6th CLP group served as untreated control. Western blotting, enzyme-linked immunosorbent assay (ELISA) and real-time quantitative polymerase chain reaction (qRT-PCR) were used for the assessment of the expression levels of tumor necrosis factor-α (TNF- α), interleukn-6 (IL-6), nucleotide-binding oligomerization domain 2 (NOD2) and p-NF-κB p65. Results: Cecal ligation and puncture (CLP) significantly and time-dependently upregulated the expressions of TNF-α, IL-6 and NOD2 in intestinal tissues of rats (p < 0.05). However, treatment with floroindole significantly, and dose-dependently down-regulated CLP-induced expressions of these proteins (p < 0.05). Treatment of rats with floroindole also significantly and dose-dependently inhibited CLP-induced phosphorylation of NF-κB p65 in rat ileum (p < 0.05). Conclusion: The results obtained in this study demonstrate that floroindole confers some degree of protection against CLP-induced sepsis via inhibition of NF-κB p65 phosphorylation.

The enigmatic role of TIPE2 in asthma

2020 ◽  
Vol 319 (1) ◽  
pp. L163-L172
Author(s):  
Bingqing Shi ◽  
Yuqiu Hao ◽  
Wei Li ◽  
Hongna Dong ◽  
Mengting Xu ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Inflammatory Cells ◽  
Underlying Mechanism ◽  
Cell Receptor ◽  
Asthma Phenotypes ◽  
Downstream Signaling ◽  
Tnf Α ◽  
And Function ◽  
Necrosis Factor

Unlike other members of the tumor necrosis factor (TNF)-α-induced protein 8 (TNFAIP8/TIPE) family that play a carcinogenic role and regulate apoptosis, TNFAIP8-like 2 (TIPE2) can not only maintain immune homeostasis but also regulate inflammation. TIPE2 mainly restrains the activation of T cell receptor (TCR) and Toll-like receptors (TLR), regulating its downstream signaling pathways, thereby regulating inflammation. Interestingly, TIPE2 is abnormally expressed in many inflammatory diseases and may promote or inhibit inflammation in different diseases. This review summarizes the molecular target and cellular function of TIPE2 in immune cells and inflammatory diseases and the underlying mechanism by which TIPE2 regulates inflammation. The function and mechanism of TIPE2 in asthma is also explained in detail. TIPE2 is abnormally expressed in asthma and participates in the pathogenesis of different phenotypes of asthma through regulating multiple inflammatory cells’ activity and function. Considering the indispensable role of TIPE2 in asthma, TIPE2 may be an effective therapeutic target in asthma. However, the available data are insufficient to provide a full understanding of the complex role of TIPE2 in human asthma. Further study is still necessary to explore the possible mechanism and functions of TIPE2 in different asthma phenotypes.

High Fibular Osteotomy Ameliorates Medial Compartment Knee Osteoarthritis in a Rabbit Model

2021 ◽  
Author(s):  
Feihua Yan ◽  
Xujun Zhao ◽  
Shisheng Duan ◽  
Aini Maimaiti ◽  
Yong Qi ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Knee Osteoarthritis ◽  
Bone Remodeling ◽  
Western Blotting ◽  
Subchondral Bone ◽  
Rabbit Model ◽  
Medial Compartment ◽  
Enzyme Linked Immunosorbent Assay ◽  
Fibular Osteotomy ◽  
Tnf Α

Abstract Purpose Knee osteoarthritis (KOA) is a common and severe disease characterized by articular cartilage degeneration, subchondral bone remodeling and inflammation. This study aimed to investigate the therapeutic effects of high fibular osteotomy (HFO) in a KOA rabbit model and to examine the molecular mechanisms involved in medial compartment KOA protective effects.Methods A rabbit model of destabilization of the medial meniscus was used to induce post-traumatic KOA. The effectiveness of HFO on protection against KOA was tested. Hematoxylin and eosin staining, Safranin O/Fast green staining and micro-CT analysis were performed to evaluate structural and morphological changes. The expression of metalloproteinase (MMP)-1, MMP-3, MMP-13, collagen type II (Col2), a disintegrin and metalloproteinase domain with thrombospondin motifs (ADAMTS)-5, aggrecan, interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α was assessed by real time PCR, western blotting and enzyme-linked immunosorbent assay. Additionally, western blotting was performed to test the expression of NFκB p65, phospho-IκBα and IκBα. Results HFO delayed the progression of articular cartilage damage and suppressed subchondral bone remodeling. HFO also decreased MMP-1, MMP-3, MMP-13 and ADAMTS-5 expression, and increased Col2 and aggrecan expression. In parallel, HFO attenuated the expression of IL-1β, IL-6 and TNF-α. Furthermore, the molecular mechanism underlying the protective effect of HFO in medial compartment KOA was related to the NFκB signaling pathway. Conclusion HFO may be a novel therapeutic approach to treating medial compartment KOA.

scholarly journals Yan-Hou-Qing formula attenuates ammonia-induced acute pharyngitis in rats via inhibition of NF-κB and COX-2

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Min Xu ◽  
Tian-Yong Hu ◽  
Dong-Cai Li ◽  
Li Ma ◽  
Hua Zhang ◽  
...  
Keyword(s):  
Inflammatory Cells ◽  
Underlying Mechanism ◽  
Control Group ◽  
Model Group ◽  
Rat Models ◽  
Acute Pharyngitis ◽  
Histopathologic Study ◽  
Tnf Α ◽  
Protein Expressions ◽  
Cox 2

Abstract Background Yan Hou Qing (YHQ) is a Chinese medicinal formula designed to alleviate sore throat symptoms, but underlying mechanism of YHQ treatment for pharyngitis is poorly defined up to now. Methods In this study, the modulation of YHQ on pharyngitis is investigated in ammonia-induced acute pharyngitis rat models. After treatment with YHQ or dexamethasone respectively for five consecutive days, all rats were sacrificed for biomolecular and histopathologic study. Protein expressions of MAPKs, NF-κB, COX-2 and 5-LOX in pharyngitis tissue were evaluated by western blot analysis and the levels of TNF-α, IL-6, prostaglandin (PG) E2, leukotrienes (LT)-B4 and LT-D4 in pharyngeal tissue were measured via ELISA assay. Evans blue (EB) dye exudation test was performed parallelly to assess the integrity of pharyngeal tissue. Results Compared with normal control group, EB dye exudation, and inflammatory cytokines in the model group were significantly increased, and the pharynx tissue was obviously infiltrated by inflammatory cells. YHQ treatment improved the inflammatory infiltrate in pharyngeal tissue, and reduced EB dye exudation in AP rat models. The up-regulated TNF-α and IL-6 in pharyngeal tissue of AP were significantly reduced by YHQ through inhibition of phosphorylation of p38, Erk and NF-κB. YHQ treatment also reversed the increased level of PGE2 through down-regulation of COX-2. Conclusions YHQ formula attenuated the pharyngitis related symptoms via suppression of COX-2 and phosphorylation of p38, Erk and NF-κB (p65).

Correlation between Depression, Posttraumatic Stress Disorder, and Inflammatory Factors in Patients with Severe Burn Injury

2018 ◽  
Vol 84 (8) ◽  
pp. 1350-1354 ◽  
Author(s):  
Donglin Jiang ◽  
Shengyang Jiang ◽  
Fang Gong ◽  
Fenglai Yuan ◽  
Peng Zhao ◽  
...  
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Disorder ◽  
Burn Injury ◽  
Self Report ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Severe Burn ◽  
Tnf Α ◽  
Severe Burn Injury

We aim to investigate the relation between depression, posttraumatic stress disorder (PTSD), and inflammatory factors in patients with severe burn injury. Psychological assessment was carried out using PTSD checklist (PCL) involving a 17-item self-report questionnaire (PCL-17) and the Hamilton Rating Scale for depression (HAMD-24). The serum IL-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) were determined using enzyme-linked immunosorbent assay. Correlation analysis was performed to analyze the correlation between the factors and scores of PTSD and depression. Compared with the PCL-17 score, HAMD-24 score, and inflammatory factors at month 3, a significant decrease was noticed in the PCL-17 score, HAMD-24 score, and inflammatory factors at months 6 and 9 (P < 0.01). For the HAMD-24 score, significant improvements were noticed in the anxiety/somatization, cognitive disorder, blocking, sleep disorders, and depression at months 3, 6, and 9. The levels of IL-1β, IL-8, and TNF-α were positively correlated with the PCL-17 score (P < 0.05). The levels of IL-1β, IL-6, IL-8, and TNF-α were positively correlated with the HAMD-24 score (P < 0.05). Patients with severe burn injury showed obvious stress alternation displaying specific depression-related characteristics, and inflammation may involve in the pathogenesis of PTSD and depression in burn patients.

scholarly journals High YKL-40 serum levels and its expression in the muscle tissues of patients with antisynthetase syndrome

2021 ◽  
Vol 61 (1) ◽  
Author(s):  
Renata Casseb de Souza Carboni ◽  
Gustavo Luiz Behrens Pinto ◽  
Samuel Katsuyuki Shinjo
Keyword(s):  
Clinical Laboratory ◽  
Disease Status ◽  
Inflammatory Cells ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Antisynthetase Syndrome ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Muscle Tissues ◽  
Tnf Α

Abstract Background The protein chitinase-3-like-1 (YKL-40) is rarely analyzed in patients with myositis. Therefore, we aimed to evaluate YKL-40 serum levels; correlate them with laboratory and clinical parameters, disease status, and treatment schemes; and analyze the YKL-40 expression in the muscle tissues of patients with antisynthetase syndrome (ASSD). Methods This cross-sectional single-center study included 64 adult patients with ASSD who were age-, gender-, and ethnicity-matched to 64 healthy control individuals. Their YKL-40 serum levels were analyzed using the Enzyme-Linked Immunosorbent Assay (ELISA) kit method, while YKL-40 expression in muscle tissues was analyzed using an immunohistochemical technique. Disease status was assessed using the International Myositis Assessment and Clinical Studies Group (IMACS) set scores. Results The patients’ mean age was 44.8 ± 11.8 years, and median disease duration was 1.5 (0.0–4.0) years. These patients were predominantly female (82.8%) and Caucasian (73.4%). Most patients had stable disease. The median YKL-40 serum level was significantly higher in patients with ASSD when compared to the healthy individuals: 538.4 (363.4–853.1) pg/mL versus 270.0 (201.8–451.9) pg/mL, respectively; P < 0.001. However, YKL-40 serum levels did not correlate with any clinical, laboratory, disease status, or therapeutic parameters (P > 0.050), except tumor necrosis factor alpha (TNF-α) serum levels (Spearman’s correlation, rho = 0.382; P = 0.007). YKL-40 was highly expressed by inflammatory cells found in muscle biopsy specimens. Conclusions High YKL-40 serum levels were observed in patients with ASSD and correlated positively with TNF-α serum levels. Moreover, YKL-40 was expressed by the inflammatory cells of the muscle tissue.

scholarly journals Acupuncture Can Regulate the Peripheral Immune Cell Spectrum and Inflammatory Environment of the Vascular Dementia Rat, and Improve the Cognitive Dysfunction of the Rats

2021 ◽  
Vol 13 ◽  
Author(s):  
Pan Pan ◽  
Zhinan Ma ◽  
Zhen Zhang ◽  
Zhenzhen Ling ◽  
Yao Wang ◽  
...  
Keyword(s):  
Immune Function ◽  
Vascular Dementia ◽  
Cognitive Dysfunction ◽  
Peripheral Blood ◽  
Acupuncture Treatment ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Spatial Learning And Memory ◽  
Tnf Α ◽  
Cox 2

ObjectiveThe aim of this study is to analyze the effects of acupuncture on peripheral immune function, inflammation, and cognitive impairment in vascular dementia (VD) rats.MethodsIn this study, 2-month-old healthy male Wistar rats (260–280 g) were assigned to the groups as follows: normal group (Gn, n = 10), sham-operated group (Gs, n = 10), and operated group (Go, n = 45). The Go group was established by permanent, bilateral common carotid artery occlusion (BCCAO). Two months after operation, the operated rats were screened by hidden platform trial and the rats with cognitive dysfunction were further randomly divided into impaired group (Gi), acupoint group (Ga), and non-acupoint group (Gna) with 10 rats in each group. The Ga group was given acupuncture treatment for 14 days with a rest for every 7 days. After treatment, the Morris water maze (MWM) test was performed to evaluate the spatial learning and memory abilities of rats. The lymphocyte subsets in peripheral blood and spleen of rats were measured by flow cytometry. The levels of cytokines [i.e., interleukin (IL)-1β, IL-2, IL-4, IL-10, tumor necrosis factor-α (TNF-α), and interferon-γ (INF-γ)], chemokines (i.e., macrophage inflammatory protein-2 (MIP-2)), and other inflammatory mediators (i.e., cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS)) in peripheral blood and hippocampus were measured by enzyme linked immunosorbent assay (ELISA).ResultsCompared with the Gn group, the Gi rats presented long escape latencies to find the platform. After acupuncture treatment, the escape latencies of the Ga group were rescued markedly when compared with the Gi group (P &lt; 0.05). The proportion of CD4 + T lymphocytes in both spleen and peripheral blood in the Ga group increased (P &lt; 0.05) in comparison with the Gi group. There is an obvious reduction in IL-1β (P &lt; 0.05), IL-2 (P &lt; 0.05), TNF-α (P &lt; 0.01), INF-γ (P &lt; 0.01), MIP-2 (P &lt; 0.05), and iNOS (P &lt; 0.01), coming along with the increased levels of IL-4 and IL-10 (P &lt; 0.01) in the Ga group when compared with the Gi group. In addition, the hippocampus proinflammatory factors IL-1β (P &lt; 0.01), IL-2 (P &lt; 0.01), TNF-α (P &lt; 0.05), INF-γ (P &lt; 0.05), MIP-2 (P &lt; 0.05), iNOS (P &lt; 0.01), and COX-2 decreased in the Ga group, whereas the anti-inflammatory factors IL-4 and IL-10 (P &lt; 0.01) increased.ConclusionThere are abnormal immune function and peripheral inflammation in VD rats. Acupuncture can regulate the peripheral immune function and inflammation of the VD rats and can improve the cognitive dysfunction of the rats.

scholarly journals Effects of IQW and IRW on Inflammation and Gut Microbiota in ETEC-Induced Diarrhea

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Naiyuan Liu ◽  
Lingsi Zhou ◽  
Jun Fang ◽  
Hongmei Jiang ◽  
Gang Liu
Keyword(s):  
Gut Microbiota ◽  
Inflammatory Cytokines ◽  
Shannon Index ◽  
Community Diversity ◽  
Enterotoxigenic Escherichia Coli ◽  
Enzyme Linked Immunosorbent Assay ◽  
Crypt Depth ◽  
Tnf Α ◽  
Group B ◽  
Gut Damage

Background/Aims. Changing gut microbiota is one of the most common causes of host gut inflammation. The active triple peptides, lle-Gln-Trp (IQW) and lle-Arg-Trp (IRW), cause remarkable changes to gut microbiota. The effects of the triple peptides IQW and IRW in gut-damage treatment were explored in this study via an enterotoxigenic Escherichia coli- (ETEC-) induced mouse model. Methods. The mice were randomly distributed into four groups: (a) control (CTRL) group, (b) ETEC group, (c) IQW-ETEC group, and (d) IRW-ETEC group. Villus length and crypt depth were measured after hematoxylin and eosin staining. The inflammatory reaction was analyzed via inflammatory cytokines (i.e., TNF-α, IL-1β, IL-6, and IL-10) using the enzyme-linked immunosorbent assay (ELISA). The microbiota in the colon was sequenced using 16S ribosomal RNA. Results. The villus length decreased, the crypt depth decreased, and the expression of inflammatory cytokines (i.e., TNF-α, IL-1β, IL-6, and IL-10) increased due to ETEC. In the IRW-ETEC and IQW-ETEC groups, the Shannon index decreased ( P < 0.05 ). IQW and IRW increased the abundance of Firmicutes, Proteobacteria, Clostridiales, Lachnospiraceae, and Alloprevotella; contrastingly, it decreased the abundance of Epsilonproteobacteria, Erysipelotrichales, Prevotellaceae, and Flavobacteriaceae compared to the ETEC group (P <0.05). Conclusion. This study ascertained that the addition of IQW and IRW could alleviate jejunal inflammation and increase microbiota community diversity.

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