scholarly journals Antiulcerogenic Activity of Li-Zhong Decoction on Duodenal Ulcers Induced by Indomethacin in Rats: Involvement of TLR-2/MyD88 Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Houpan Song ◽  
Meiyan Zeng ◽  
Xiaojuan Chen ◽  
Xinyi Chen ◽  
Jun Peng ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Duodenal Mucosa ◽  
Interleukin 4 ◽  
Prostaglandin E ◽  
Sprague Dawley ◽  
Serious Adverse Events ◽  
Inflammatory Infiltration ◽  
Expression Levels ◽  
Anti Inflammatory ◽  
Myd88 Signaling

Background. Administration of nonsteroidal anti-inflammatory drugs (NSAIDs) often causes small intestinal ulcers in patients, but few effective drugs are currently available to manage such serious adverse events of NSAIDs. Li-Zhong decoction (LZD), a well-known traditional Chinese medicine (TCM) formula, is commonly prescribed for treatment of gastrointestinal diseases. The present study aimed to investigate the anti-ulcerogenic activity of LZD on indomethacin- (IND-) induced duodenal ulcer in rats. Mechanistic studies of action of LZD were focused on involvement of TLR-2/MyD88 signaling pathway. Methods. Fifty male Sprague-Dawley (SD) rats were randomly and evenly divided into five groups: normal control, ulcer control (IND, 25 mg/kg), IND + esomeprazole (ESO, 4.17 mg/kg), and IND + low and high doses of LZD (3.75 and 7.50 g/kg). Macroscopic and histopathological examinations were performed for evaluation of ulcer index (UI), curative index (CI), and microscopic score (MS). Levels of duodenal inflammatory biomarkers and cytoprotective mediators including interleukin-4 (IL-4), IL-10, tumor necrosis factor-α (TNF-α), and prostaglandin E2 (PGE2) were measured by ELISA. Expression levels of TLR-2 and MyD88 mRNA were assessed by qRT-PCR. The expression and distribution of TLR-2 and MyD88 proteins were analyzed by western blot and immunohistochemistry, respectively. Results. Gross and microscopic examinations of the IND-treated rats revealed severe duodenal hemorrhagic necrosis, inflammatory infiltration, villus destruction, and crypt abscess, while LZD-treated rats manifested these pathological events to a markedly lesser degree. LZD significantly decreased UI and MS, increased CI, preserved the integrity of the villus and crypt, and normalized the tissue architecture of the duodenum of rats. The elevated TNF-α levels in the IND-treated rats were markedly diminished in the LZD-treated rats, while lower levels of IL-4, IL-10, and PGE2 observed in IND-treated rats were significantly increased in LZD-treated rats. Interestingly, improvement of immune function in duodenal mucosa by reduction of mRNA and protein expression levels of TLR-2 and MyD88 was also observed in rats treated with LZD. Consistently, immunohistochemical analyses revealed a lower co-localization of TLR-2 and MyD88 proteins in the duodenal mucosa of LZD-treated rats as compared to the IND-induced rats. Conclusions. Our data demonstrate that LZD protects the duodenal mucosa from IND-caused lesions, which is at least partially attributable to the interaction of its potential cytoprotective and anti-inflammatory mechanisms together with enhancement of the mucosal immunity through TLR-2/MyD88 signaling pathway.

scholarly journals Hydro ethanol extract of Holarrhena floribunda stem bark exhibits anti-anaphylactic and anti-oedematogenic effects in murine models of acute inflammation

2020 ◽  
Author(s):  
Stephen Antwi ◽  
Daniel Oduro-Mensah ◽  
David Darko Obiri ◽  
Newman Osafo ◽  
Aaron Opoku Antwi ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Serotonin Receptor ◽  
Acute Inflammation ◽  
Late Phase ◽  
Ethanol Extract ◽  
Stem Bark ◽  
Bark Extract ◽  
Prostaglandin E ◽  
Sprague Dawley ◽  
Anti Inflammatory

Abstract Background: Holarrhena floribunda stem bark has anecdotal use in Ghanaian folk medicine for management of inflammatory conditions. This study was conducted to investigate the in vivo anti-inflammatory activity of the bark extract using models of acute inflammation in male Sprague Dawley rats, C57BL/6 mice and 36 ICR mice. Methods: A 70 % hydro-ethanol extract of the stem bark (HFE) was evaluated at doses of 5–500 mg/kg bw. Local anaphylaxis was modelled by the pinnal cutaneous anaphylactic test. Systemic anaphylaxis or sepsis were modeled by compound 48/80 or lipopolysaccharide, respectively. Clonidine-induced catalepsy was used to investigate effect on histamine signaling. Anti-oedematogenic effect was assessed by induction with carrageenan. Effects on mediators of biphasic acute inflammation were studied using histamine and serotonin (early phase) or prostaglandin E2 (late phase).Results: HFE demonstrated anti-inflammatory and/or anti-oedematogenic activity comparable to standard doses of aspirin and diclofenac (inhibitors of cyclooxygenases-1 and -2), chlorpheniramine (histamine H1-receptor antagonist), dexamethasone (glucocorticoid receptor agonist), granisetron (serotonin receptor antagonist) and sodium cromoglycate (inhibitor of mast cell degranulation). All observed HFE bioactivities increased with dose.Conclusions: The data provide evidence that the extract of H. floribunda stem bark has anti-anaphylactic and anti-oedematogenic effects; by interfering with signalling or metabolism of histamine, serotonin and prostaglandin E2 which mediate progression of inflammation. The anti-inflammatory and antihistaminic activities of HFE may be relevant in the context of management of COVID-19.

scholarly journals An Anti-Inflammatory Composition of Boswellia serrata Resin Extracts Alleviates Pain and Protects Cartilage in Monoiodoacetate-Induced Osteoarthritis in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Venkata Krishnaraju Alluri ◽  
Sreenath Kundimi ◽  
Krishanu Sengupta ◽  
Trimurtulu Golakoti ◽  
Eswar Kumar Kilari
Keyword(s):  
Articular Cartilage ◽  
Structural Damage ◽  
Weight Bearing ◽  
Prostaglandin E ◽  
Thermal Stimulus ◽  
Sprague Dawley ◽  
Boswellia Serrata ◽  
Anti Inflammatory ◽  
Safranin O ◽  
Unique Composition

The boswellic acids, the active compounds in Boswellia serrata gum resin extract, are potent anti-inflammatory agents and are specific nonredox inhibitors of 5-Lipoxygenase (5-LOX). Here, we present the anti-osteoarthritis (OA) efficacy of LI13019F1 (also known as Serratrin®), a unique composition containing the acidic and nonacidic fractions of B. serrata gum resin. This composition strongly inhibited 5-LOX activity with the half-maximal inhibitory concentration (IC50) of 43.35 ± 4.90 μg/mL. Also, LI13019F1 strongly inhibited the leukotriene B4 (IC50, 7.80 ± 2.40 μg/mL) and prostaglandin E2 (IC50, 6.19 ± 0.52 μg/mL) productions in human blood-derived cells. Besides, LI13019F1 reduced TNF-α production with the IC50 of 12.38 ± 0.423 μg/mL. On average, 1, 2.5, and 5 μg/mL doses of LI13019F1 protected 34.62, 47.66, and 62.29% SW1353 human chondrosarcoma cells from IL-1β induced SOX-9 depletion, respectively. Further, a 28-day preclinical proof-of-concept study evaluated the pain relief efficacy of LI13019F1 in monoiodoacetate- (MIA-) induced Sprague-Dawley rats. At the end of the study, 150 and 300 mg/kg doses of LI13019F1 supplemented rats showed significant improvements (55.17 ± 5.81 g (p<0.05), and 66.22 ± 6.30 g (p<0.05), respectively, vs. MIA: 31.22 ± 7.15 g) in body-weight-bearing capacities. Concurrently, LI13019F1-150 and LI13019F1-300 rats substantially (p<0.05) increased the threshold of pain sensitivity to pressure (26.98 ± 2.36 and 28.06 ± 2.72-gram force, respectively; vs. 18.63 ± 5.82 in MIA) and increased (p<0.05) the latent time to withdraw the paw after a thermal stimulus (23.61 ± 2.73 and 28.18 ± 1.90 sec, respectively; vs. 16.56 ± 1.22 sec. in MIA). Besides, the histological observations on Safranin-O green stained articular cartilage revealed that LI13019F1 also prevented the MIA-induced structural damage of the cartilage and reduced the loss of the extracellular matrix (ECM) components in the experimental rats. In conclusion, the present observations suggest that LI13019F1, a new composition of B. serrata gum resin extracts, reduces pain and protects articular cartilage from the damaging action of MIA in a rodent model.

scholarly journals Protective Effects of Anwulignan against HCl/Ethanol-Induced Acute Gastric Ulcer in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Jiawei Liu ◽  
Huijiao Lin ◽  
Liwei Yuan ◽  
Dan Wang ◽  
Chunmei Wang ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Signaling Pathway ◽  
Interleukin 2 ◽  
Gastrointestinal Diseases ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Gastric Ulcers ◽  
Protective Effects ◽  
Gastric Tissue ◽  
Anti Inflammatory

Gastric ulcer is one of the most common gastrointestinal diseases. Anwulignan (AN) is a major active component of Schisandra sphenanthera Rehd. This study was designed to evaluate the protective effect of AN against the acute gastric ulcer induced by HCl/ethanol in mice. The mice were given HCl/ethanol by gavage to establish an acute gastric ulcer model. Then, the serum and gastric tissue samples were taken for biochemical analyses. The results showed that the pretreatment with AN could significantly reduce the gastric ulcer index (GUI) and increase the ulcer inhibition rate, indicating that AN can protect against gastric ulcers. AN showed its antioxidant roles by decreasing the content of reactive oxygen species (ROS), malondialdehyde (MDA), and 8-hydroxydeoxyguanosine (8-OHdG) and increasing the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) and anti-inflammatory roles by decreasing the content of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and myeloperoxidase (MPO) and increasing the content of interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-10 (IL-10), prostaglandin E2 (PGE2), and nitric oxide (NO) in both serum and gastric tissue. Furthermore, AN also activated the NRF2/ARE signaling pathway and inhibited the MAPK/NF-κB signaling pathway. AN improves the acute gastric ulcer induced by HCl/ethanol in mice, which may be mainly through its antioxidant capacity and anti-inflammatory effect.

scholarly journals Schisandra chinensis extract ameliorates myocardial ischemia/reperfusion injury via TLR4/NF-κB/MyD88 signaling pathway

2020 ◽  
Vol 19 (1) ◽  
pp. 57-62
Author(s):  
Yang Lou ◽  
Bo Xu ◽  
Xianshuai Li ◽  
Xiaoyi Xu ◽  
Xiaoguo Chen
Keyword(s):  
Signaling Pathway ◽  
Myocardial Infarct ◽  
Enzyme Linked Immunosorbent Assay ◽  
Myocardial Infarct Size ◽  
Schisandra Chinensis ◽  
Protective Effects ◽  
Triphenyltetrazolium Chloride ◽  
Sod Activity ◽  
Expression Levels ◽  
Myd88 Signaling

Purpose: To investigate the effects of Schisandra chinensis extract (SCE) on myocardial ischemiareperfusion (I/R) injury and to elucidate its underlying mechanism of action. Methods: A rat model of myocardial I/R injury was used. Ischemia was induced by occluding the left anterior descending artery for 30 min and the myocardium was then reperfused for 2 h in Sprague-Dawley rats. Triphenyltetrazolium chloride (TTC) staining was used to measure myocardial infarct size, while the levels of inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay (ELISA). Western blot assay was conducted to determine protein levels. Results: TTC staining showed that myocardial I/R injury was ameliorated after SCE treatment. Serum creatine kinase (CK), lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels decreased, whereas superoxide dismutase (SOD) activity increased after SCE treatment. Moreover, seruminterleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) expression levels were reduced after SCE treatment. Furthermore, SCE treatment remarkably downregulated the protein expression levels of Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), and myeloid differentiation factor 88 (MyD88). Conclusion: SCE may exert protective effects against myocardial I/R injury by downregulating TLR4-mediated NF-κB/MyD88 signaling pathway. However, this needs to confirmed in clinical studies. Keywords: Schisandra chinensis, TLR4/NF-κB/MyD88, Inflammasome, Myocardial ischemiareperfusion injury

scholarly journals Anti-Inflammatory Effect of Piper attenuatum Methanol Extract in LPS-Stimulated Inflammatory Responses

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
You Jin Kim ◽  
Jeong Deok ◽  
Sunggyu Kim ◽  
Deok Hyo Yoon ◽  
Gi-Ho Sung ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Intracellular Signaling ◽  
Methanol Extract ◽  
Inflammatory Responses ◽  
Mechanisms Of Action ◽  
No Synthase ◽  
Poly I:C ◽  
Prostaglandin E ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Piper attenuatum is used as a traditional medicinal plant in India. One of the substances in P. attenuatum has been suggested to have anti-inflammatory effects. However, there is insufficient research about the anti-inflammatory mechanisms of action of P. attenuatum. The effects of P. attenuatum methanol extract (Pa-ME) on the production of inflammatory mediators nitric oxide (NO) and prostaglandin E2 (PGE2), the expression of proinflammatory genes, the translocation level of transcription factors, and intracellular signaling activities were investigated using macrophages. Pa-ME suppressed the production of NO and PGE2 in lipopolysaccharide- (LPS-), pam3CSK4-, and poly(I:C)-stimulated RAW264.7 cells without displaying cytotoxicity. The mRNA expression levels of inducible NO synthase (iNOS) and cyclooxygenase 2 (COX-2) were decreased by Pa-ME. P-ME reduced the translocation of p50/NF-κB and AP-1 (c-Jun and c-Fos), as well as the activity of their upstream enzymes Src, Syk, and TAK1. Immunoprecipitation analysis showed failure of binding between their substrates, phospho- (p-) p85 and p-MKK3/6. p-p85 and p-MKK3/6, which were induced by overexpression of Src, Syk, and TAK1, were also reduced by Pa-ME. Therefore, these results suggest that Pa-ME exerts its anti-inflammatory effects by targeting Src and Syk in the NF-κB signaling pathway and TAK1 in the AP-1 signaling pathway.

scholarly journals Andrographolide Inhibits Inflammatory Cytokines Secretion in LPS-Stimulated RAW264.7 Cells through Suppression of NF-κB/MAPK Signaling Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yu Li ◽  
Shengnan He ◽  
Jishun Tang ◽  
Nana Ding ◽  
Xiaoyan Chu ◽  
...  
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Proinflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Raw264.7 Cells ◽  
Nuclear Level ◽  
Expression Levels ◽  
Anti Inflammatory

Andrographolide, the main active component extracted from Andrographis paniculata (Burm.f.) Wall. ex Nees, exerts anti-inflammatory effects; however, the principal molecular mechanisms remain unclear. The objective of this study was to investigate the molecular mechanisms of Andrographolide in modifying lipopolysaccharide- (LPS-) induced signaling pathway in RAW264.7 cells. An in vitro model of inflammation was induced by LPS in mouse RAW264.7 cells in the presence of Andrographolide. The concentration and expression levels of proinflammatory cytokines were determined by an enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. The nuclear level of NF-κB was measured by an electrophoretic mobility shift assay (EMSA). The expression levels of NF-κB, p38, ERK, and JNK were determined by western blot. Andrographolide dose-dependently inhibited the release and mRNA expression of TNF-α, IL-6, and IL-1β in LPS-stimulated RAW264.7 cells. The nuclear level of p65 protein was decreased in Andrographolide treatment group. Western blot analysis showed that Andrographolide suppressed LPS-induced NF-κB activation and the phosphorylation of IkBa, ERK1/2, JNK, and p38. These results suggest that Andrographolide exerts an anti-inflammatory effect by inhibiting the activation of NF-κB/MAPK signaling pathway and the induction of proinflammatory cytokines.

scholarly journals Role of Artesunate on cardiovascular complications in rats with type 1 diabetes mellitus

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yi Chen ◽  
Wei Li ◽  
Xiaolin Nong ◽  
Chen Liang ◽  
Jiaquan Li ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Aortic Arch ◽  
Signaling Pathway ◽  
Blood Lipid ◽  
Cardiovascular Complications ◽  
Diabetic Rats ◽  
Inflammatory Factors ◽  
Sprague Dawley ◽  
Expression Levels

Abstract Background The present study aimed to evaluate the effect of artesunate (ART) on the reduction of cardiovascular complications in a type 1 diabetes model and to investigate the associated mechanism based on the receptor for advanced glycation end-product (RAGE)/NF-κB signaling pathway. Methods A total of 40 male Sprague-Dawley rats were randomly divided into five groups: The healthy, diabetic, 50 mg/kg ART (ig) treatment diabetic, 100 mg/kg ART (ig) treatment diabetic, and 6 U/kg insulin (iH) treatment diabetic groups. The treatment lasted 4 weeks after the diabetic model was established via intraperitoneal injection of streptozotocin. Blood samples were collected, and cardiovascular tissues were harvested and processed to measure various parameters after the animals were sacrificed. The myocardium and aortic arch tissues were evaluated using hematoxylin-eosin and Masson staining. Expression levels of RAGE, NF-κB, matrix metalloproteinase MMP9, MMP1 and CD68 in the myocardium and aortic arch tissues were detected using immunohistochemistry, and mRNA expression was determined using reverse transcription-quantitative PCR. Results The results of the present study demonstrated that ART treatment may restrain diabetes-induced cardiovascular complications by maintaining heart and body weight while reducing blood glucose, as well as regulating blood lipid indicators to normal level (P < 0.05). The expression levels of NF-κB, CD68, MMP1, MMP9 and RAGE were decreased in the ART-treated diabetic rats (P < 0.05). Conclusions ART treatment may have a protective role against diabetes-associated cardiovascular complications in diabetic rats by inhibiting the expression of proteins in the RAGE/NF-κB signaling pathway and downstream inflammatory factors. High concentrations of ART had a hypoglycemic effect, while a low concentration of ART prevented cardiovascular complications.

scholarly journals Anemoside B4 protects against Klebsiella pneumoniae- and influenza virus FM1-induced pneumonia via the TLR4/Myd88 signaling pathway in mice

2020 ◽  
Author(s):  
Jia He ◽  
Renyikun Yuan ◽  
Xiaolan Cui ◽  
Yushun Cui ◽  
Shan Han ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Molecular Docking ◽  
Signaling Pathway ◽  
Therapeutic Effect ◽  
Inflammatory Cytokines ◽  
Inflammatory Activity ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Myd88 Signaling ◽  
Pro Inflammatory Cytokines

Abstract Background: Pneumonia refers to the inflammation of the terminal airway, alveoli and pulmonary interstitium, which can be caused by pathogenic microorganisms, physical and chemical factors, immune damage, and drugs. Anemoside B4, the major ingredient of Pulsatilla chinensis (Bunge) Regel, exhibited anti-inflammatory activity. However, the therapeutic effect of anemoside B4 on pneumonia has not been unraveled. This study aims to investigate that anemoside B4 attenuates the inflammatory responses in Klebsiella pneumonia (KP)- and influenza virus FM1 (FM1)-induced pneumonia mice model.Methods: The network pharmacology and molecular docking assays were employed to predict the targets of anemoside B4’s treatment of pneumonia. Two models (bacterial KP-infected mice and virus FM1-infected mice) were employed in our study. BALB/c mice were divided into six groups: control, model group (KP- induced pneumonia or FM1-induced pneumonia), anemoside B4 (B4)-treated group (2.5, 5, 10 mg/kg), and positive drug group (Ribavirin or Ceftriaxone Sodium Injection). Blood samples were collected for hematology analysis. The effects of B4 on inflammation-associated mediators were investigated by Enzyme-linked immunosorbent assay (ELISA) and hematoxylin and eosin staining (HE) staining. Proteins expression was quantified by western blotting.Results: The network results indicated that many pro-inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) participated in anemoside B4’s anti-inflammatory activity. The counts of neutrophil (NEU) and white blood cell (WBC), the level of myeloperoxidase (MPO), and the release of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 increased by KP or FM1 infection, which were reversed by anemoside B4. In addition, anemoside B4 significantly suppressed the FM1-induced expression of Toll-like receptor 4 (TLR4), myeloid differential protein-88 (MyD88), and myeloid differentiation protein-2 (MD-2), which were further validated by molecular docking data that anemoside B4 bound to bioactive sites of TLR4. Therefore, anemoside B4 exhibited a significant therapeutic effect on pneumonia via the TLR4/MyD88 pathway.Conclusion: Our findings demonstrated that anemoside B4 attenuates pneumonia via the TLR4/Myd88 signaling pathway, suggesting that anemoside B4 is a promising therapeutic candidate for bacterial-infected or viral-infected pneumonia.

scholarly journals Inhibitory Effects of Camellia Japonica on Cell Inflammation and Acute Rat Reflux Esophagitis

2020 ◽  
Author(s):  
Hyeon Hwa Nam ◽  
Li Nan ◽  
Byung Kil Choo
Keyword(s):  
Reflux Esophagitis ◽  
Radical Scavenging ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Camellia Japonica ◽  
Expression Levels ◽  
Natural Medicine ◽  
Esophageal Tissue ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Background Excessive and continuous inflammation may be the main cause of various immune system diseases. Reflux esophagitis (RE) is a common gastroesophageal reflux disease (GERD). It is an inflammation of the esophagus caused by the reflux of gastric contents to the esophagus due to the dysfunction of the lower esophageal sphincter. Camellia japonica has high medicinal value and has long been used as a traditional herbal hemostatic medicine in China and Korea. Materials and methods Dried C. japonica buds were extracted with 75% ethanol. DPPH and ABTS radical scavenging assay were evaluated according to previous method. The ROS production and anti-inflammatory effects of C. japonica buds ethanol extract (CJE) were evaluated on LPS-induced RAW 264.7 macrophage cells. The protective effects of CJE on RE were conducted in a RE induced Sprague Dawley rat model. Results CJE eliminated over 50% of DPPH and ABTS radical at concentration of 100 and 200 µg/mL, respectively. CJE alleviated changes in cell morphology, reduced production of ROS, NO and IL-1β. Also, down-regulated expression levels of iNOS, TNF-α, phosphorylated NF-κB, IκBα, and JNK/p38/MAPK. CJE reduced esophageal tissue damage ratio (40.3%) and attenuation of histological changes. In addition, CJE down-regulated the expression levels of TNF-α, IL-1β, COX-2 and phosphorylation levels of NF-κB and IκBα in esophageal tissue . Conclusions CJE possesses good anti-oxidation and anti-inflammatory activity, and can improve RE in rats caused by acid reflux. Therefore, CJE may be a natural medicine source with good anti-oxidation and anti-inflammatory effects, and a candidate phytomedicine source for treating RE

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