scholarly journals Saposhnikoviae Radix Enhanced the Angiogenic and Anti-Inflammatory Effects of Huangqi Chifeng Tang in a Rat Model of Cerebral Infarction

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Qiu-Yue Wang ◽  
Na Zhang ◽  
Shu-Yu Liu ◽  
Xi-Hong Jiang ◽  
Shu-Min Liu
Keyword(s):  
Cerebral Infarction ◽  
Protein Expression ◽  
Brain Tissue ◽  
Rat Model ◽  
Cerebral Tissue ◽  
Expression Levels ◽  
Caspase 1 ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Saposhnikoviae Radix

Huangqi Chifeng Tang (HQCFT), a traditional Chinese formula of three herbs, has been used to treat cerebral infarction (CI). Saposhnikoviae Radix (SR) was designed as a guiding drug for HQCFT to improve its angiogenic and anti-inflammatory effects. In this study, TTC staining was used to detect the area of CI. H&E staining was used to detect the histopathologic changes in the cerebral tissue. Western blotting was performed to detect the protein expression of NLRP3, caspase 1, IL-1β, IL-6, TNF-α, MMP-9, VEGF, and VEGFR2 in cerebral tissue. Immunohistochemistry was used to detect the protein expression of MMP-9, VEGF, and VEGFR2. The contents of HIF-1α, NLRP3, caspase 1, IL-1β, IL-6, and TNF-α in the serum were determined by ELISA. Our study showed that HQCFT and HQCFT-SR could improve the pathological condition and reduce the infarcted area of the brain tissue in a rat model. In addition, HQCFT and HQCFT-SR significantly decreased the expression levels and serum contents of NLRP3, caspase 1, IL-1β, IL-6, and TNF-α; increased the expression levels of the VEGF and VEGFR2 proteins; and obviously reduced the serum content of HIF-1α. Importantly, the cytokines in brain tissue and serum from the HQCFT group exhibited better efficacy than those from the HQCFT-SR group. HQCFT exerted significant angiogenic and anti-inflammatory effects in rats subjected to middle cerebral artery occlusion (MCAO); these effects can be attributed to the guiding and enhancing effect of SR.

scholarly journals Pirfenidone attenuates synovial fibrosis and postpones the progression of osteoarthritis by anti-fibrotic and anti-inflammatory properties in vivo and in vitro

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qilu Wei ◽  
Ning Kong ◽  
Xiaohui Liu ◽  
Run Tian ◽  
Ming Jiao ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Fast Green ◽  
Expression Levels ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Safranin O ◽  
Tgf Β1

Abstract Background Osteoarthritis (OA) is a disease of the entire joint involving synovial fibrosis and inflammation. Pathological changes to the synovium can accelerate the progression of OA. Pirfenidone (PFD) is a potent anti-fibrotic drug with additional anti-inflammatory properties. However, the influence of PFD on OA is unknown. Methods Proliferation of human fibroblast-like synoviocytes (FLSs) after treatment with TGF-β1 or PFD was evaluated using a Cell Counting Kit-8 assay and their migration using a Transwell assay. The expression of fibrosis-related genes (COL1A1, TIMP-1, and ACTA-2) and those related to inflammation (IL-6 and TNF-α) was quantified by real-time quantitative PCR. The protein expression levels of COL1A1, α-SMA (coded by ACTA-2), IL-6 and TNF-α were measured by enzyme-linked immunosorbent assay. A rabbit model of OA was established and then PFD was administered by gavage. The expression of genes related to fibrosis (COL1A1, TIMP-1, and ADAM-12) and inflammation (IL-6 and TNF-α) was measured using RNA extracted from the synovium. Synovial tissue was examined histologically after staining with H&E, Masson’s trichrome, and immunofluorescence. Synovitis scores, the volume fraction of collagen, and mean fluorescence intensity were calculated. Degeneration of articular cartilage was analyzed using a Safranin O-fast green stain and OARSI grading. Results The proliferation of FLSs was greatest when induced with 2.5 ng/ml TGF-β1 although it did not promote their migration. Therefore, 2.5 ng/ml TGF-β1 was used to stimulate the FLSs and evaluate the effects of PFD, which inhibited the migration of FLSs at concentrations as low as 1.0 mg/ml. PFD decreased the expression of COL1A1 while TGF-β1 increased both mRNA and protein expression levels of IL-6 but had no effect on α-SMA or TNF-α expression. PFD decreased mRNA expression levels of COL1A1, IL-6, and TNF-α in vivo. H&E staining and synovitis scores indicated that PFD reduced synovial inflammation, while Masson’s trichrome and immunofluorescence staining suggested that PFD decreased synovial fibrosis. Safranin O-Fast Green staining and the OARSI scores demonstrated that PFD delayed the progression of OA. Conclusions PFD attenuated synovial fibrosis and inflammation, and postponed the progression of osteoarthritis in a modified Hulth model of OA in rabbits, which was related to its anti-fibrotic and anti-inflammatory properties.

scholarly journals Protective Effect of the Abelmoschus manihot Flower Extract on DSS-Induced Ulcerative Colitis in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Bensheng Wu ◽  
Qing Zhou ◽  
Zongqi He ◽  
Xiaopeng Wang ◽  
Xueliang Sun ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Protein Expression ◽  
Therapeutic Effect ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Colon Tissue ◽  
Expression Levels ◽  
Caspase 1 ◽  
Tnf Α ◽  
Dose Dependent

Background. The flower of Abelmoschus manihot (AM) has been widely used in the treatment of chronic inflammatory diseases, including ulcerative colitis. This paper aimed to confirm the therapeutic effect of AM on ulcerative colitis (UC) and explore its mechanism. Methods. Mouse models were induced by 2.5% dextran sulfate sodium (DSS) and treated with AM. UC signs, symptoms, colon macroscopic lesion scores, and disease activity index (DAI) scores were observed. Colon levels of interleukin- (IL-) 6, IL-1β, IL-18, IL-17, tumor necrosis factor- (TNF-) α, and IL-10 were quantified by ELISA. The colon protein expression levels of NLRP3, ASC, caspase 1 p10, β-arrestin1, ZO-1, occludin-1, and claudin-1 were examined by immunohistochemistry and western blotting. The mRNA levels of IL-1β, IL-18, NLRP3, ASC, and caspase 1 p10 in the colon were determined by real-time quantitative polymerase chain reaction (qPCR). Results. After treatment with AM, the mortality of mice, pathological damage to the colon, splenomegaly, and the spleen coefficient were decreased. AM reduced the levels of proinflammatory cytokines (IL-6, IL-1β, IL-18, IL-17, and TNF-α) and increased the level of IL-10. The mRNA expression levels of NLRP3, ASC, and caspase 1 in colon tissue were decreased by AM in a dose-dependent manner. In addition, AM also reduced the protein expression of NLRP3, ASC, caspase 1 p10, IL-1β, IL-18, and β-arrestin1 in the colon tissue of model mice. Western blot analysis confirmed that AM increased the expression of occludin-1, claudin-1, and ZO-1 in a dose-dependent manner. Conclusion. This study shows that AM has a significant therapeutic effect on mice with UC, and the mechanism may be related to the inhibition of the β-arrestin1/NLRP3 inflammasome signaling pathway and the protection of intestinal barrier function.

Thymoquinone ameliorates NLRP3-mediated inflammation in the pancreas of albino Wistar rats fed ethanol and high-fat diet

2015 ◽  
Vol 26 (6) ◽  
Author(s):  
Suguna Periyanayagam ◽  
Geetha Arumugam ◽  
Aruna Ravikumar ◽  
Vijaiyan Siva Ganesan
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Mrna Expression ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Inflammatory Activity ◽  
High Fat ◽  
Caspase 1 ◽  
Tnf Α ◽  
Anti Inflammatory

AbstractInflammasomes are protein complexes that mediate the process of inflammation and tissue injury by regulating the level of cytokine production. Pancreatitis is a major gastrointestinal disorder characterized by painful inflammation in the pancreas. The aim of this study was to evaluate whether thymoquinone (TQ) exerts anti-inflammatory activity by influencing the expression of the apoptosis-associated speck-like protein (ASC) complex of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasomes in rats subjected to experimental pancreatitis.Male albino Wistar rats were randomly separated into four groups. Rats in groups 1 and 2 were fed with a normal diet for 90 days, and rats in groups 3 and 4 were administered with ethanol (EtOH) 8–12 g/kg/day orally and fed with a high-fat diet (HFD) for 90 days. In addition, rats in groups 2 and 4 were administered with 100 mg/kg body weight of TQ from the 31st day. The serum lipase (L)/amylase (A) ratio; the oxidative stress markers; the GSH/GSSG ratio; the mRNA expression of ASC, caspase-1, IL-1β, IL-18, and TNF-α; and the protein expression of ASC and caspase-1 in the pancreas were assessed.We observed a significant increase in the serum L/A ratio and oxidative stress, a decrease in the GSH/GSSG ratio, and a GST activity in EtOH- and HFD-fed rats. The mRNA expression of IL-1β, IL-18, and TNF-α was significantly reduced in TQ-coadministered rats than that in EtOH- and HFD-fed rats. The upregulation of mRNA and the protein expression of ASC and caspase-1 were significantly reduced in TQ-coadministered rats.TQ exerts the anti-inflammatory activity probably by downregulating the ASC expression to minimize the maturation of proinflammatory cytokines.

Abstract 393: Anti-inflammatory Properties of Aqueous Extracts of Sesame Oil

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Krithika Selvarajan ◽  
Chandrakala Aluganti Narasimhulu ◽  
Reena Bapputty ◽  
Sampath Parthasarathy
Keyword(s):  
Protein Expression ◽  
Aqueous Extract ◽  
Dietary Intervention ◽  
Sesame Oil ◽  
Luciferase Assay ◽  
Treatment Modalities ◽  
Raw 264.7 Cells ◽  
Mrna Levels ◽  
Tnf Α ◽  
Anti Inflammatory

Background Dietary intervention to prevent atherosclerosis and inflammation has been a major focus in recent years. Sesame oil (SO), widely used in many Asian countries, has been reported to help reduce high blood pressure. It has also been shown to reduce plasma cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride levels. We previously reported that SO was effective in inhibiting atherosclerosis in LDL-receptor negative mice. In this study we tested whether the aqueous, non-lipid components of SO might have anti-inflammatory effects. Methods Sesame oil was extracted using ethanol:water mixture, lyophilized and reconstituted in water. To study anti-inflammatory effect, RAW 264.7 cells (macrophage cell line) were treated with the aqueous extract in the presence or absence of lipopolysaccharide (LPS) for 24 hours. RNA was extracted using Trizol. mRNA expression of inflammatory cytokines such as IL-1α, IL-6 and TNF-α were analyzed by real time PCR. Protein expression was determined by western blot analysis. To identify the mechanism of action, we performed luciferase assay using HepG2-LXR reporter cell lines. Results LPS induced the expression of IL-1α, IL-6 and TNF-α mRNA levels in RAW cells. The extract alone did not significantly affect the expressions of inflammatory cytokine genes. However, when treated together with LPS, sesame oil aqueous extract inhibited the mRNA levels of these cytokines significantly. Treatment with LPS together with SO extract also decreased the protein expression of these cytokines. The SO extract induced LXR expression as identified by the luciferase assay system in HepG2-LXR reporter cells. Conclusion These findings suggest that the aqueous portion of SO might be effective in preventing inflammation. Furthermore, the activation of LXR might suggest additional effects on lipid metabolism. Identifying the specific components present in the aqueous extract will be instrumental in developing treatment modalities for atherosclerosis and other inflammatory conditions.

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 Roles of Crosstalk between Astrocytes and Microglia in Triggering Neuroinflammation and Brain Edema Formation in 1,2-Dichloroethane-Intoxicated Mice

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2647
Author(s):  
Jinhan Yang ◽  
Tong Wang ◽  
Xiaoxia Jin ◽  
Gaoyang Wang ◽  
Fenghong Zhao ◽  
...  
Keyword(s):  
Protein Expression ◽  
Brain Edema ◽  
Adhesion Molecule ◽  
Calcium Binding ◽  
Microglial Activation ◽  
Reactive Astrocytes ◽  
Edema Formation ◽  
Expression Levels ◽  
Tnf Α ◽  
Brain Edema Formation

We have previously reported that the activation of astrocytes and microglia may lead to the overproduction of proinflammatory mediators, which could induce neuroinflammation and cause brain edema in 1,2-dichloroethane (1,2-DCE)-intoxicated mice. In this research, we further hypothesized that astrocyte–microglia crosstalk might trigger neuroinflammation and contribute to brain edema in 1,2-DCE-intoxicated mice. The present research revealed, for the first time, that subacute intoxication with 1,2-DCE might provoke the proinflammatory polarization of microglia, and pretreatment with minocycline, a specific inhibitor of microglial activation, may attenuate the enhanced protein levels of ionized calcium-binding adapter molecule1 (Iba-1), cluster of differentiation 11b (CD11b), glial fibrillary acidic protein (GFAP), soluble calcium-binding protein 100B (S100B), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase-9 (MMP-9), Toll-like receptor 4 (TLR4), MyD88, and p-p65, and ameliorate the suppressed protein expression levels of occludin and claudin 5; we also observed changes in water content and made pathological observations on edema in the brains of 1,2-DCE-intoxicated mice. Moreover, pretreatment with fluorocitrate, an inhibitor of reactive astrocytes, could also reverse the alteration in protein expression levels of GFAP, S100B, Iba-1, CD11b, TNF-α, IL-6, iNOS, VCAM-1, ICAM-1, MMP-9, occludin, and claudin 5 in the brain of 1,2-DCE intoxicated mice. Furthermore, pretreatment with melatonin, a well-known anti-inflammatory drug, could also attenuate the above-mentioned changes in the brains of 1,2-DCE-intoxicated mice. Altogether, the findings from this research indicated that microglial activation might play an important role in triggering neuroinflammation, and hence may contribute to brain edema formation; additionally, the findings suggested that molecular crosstalk between reactive astrocytes and activated microglia may amplify the neuroinflammatory reaction, which could induce secondary brain injury in 1,2-DCE-intoxicated mice.

Abstract 035: Cholinergic Agonists Protect from the Development of Hypertension during Chronic Inflammatory Disease

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Keisa W Mathis
Keyword(s):  
Protein Expression ◽  
Lupus Erythematosus ◽  
Inflammatory Diseases ◽  
Autoimmune Disorder ◽  
Chronic Inflammatory Disease ◽  
Cholinergic Agonists ◽  
Inflammatory Pathway ◽  
Genetic Mouse Model ◽  
Tnf Α ◽  
Anti Inflammatory

Systemic lupus erythematosus (SLE) is an autoimmune disorder with prevalent hypertension. Previous studies using a genetic mouse model of SLE (NZBWF1) suggest chronic inflammation is an important contributor to SLE hypertension. A novel neuroimmune pathway involving the α7 subunit of the nicotinic acetylcholine receptor (α7nAChR) suppresses splenic cytokine release and reduces systemic inflammation upon stimulation. To test whether activation of this ‘cholinergic anti-inflammatory pathway’ at the level of the α7nAChR attenuates the development of hypertension during SLE, female SLE and control (NZW) mice were infused with nicotine hydrogen tartrate salt (2 mg/kg/day, SC) or saline for 7 days. Nicotine-treated SLE mice had lower splenic protein expression of TNF-α and IL-6 (normalized to β-actin) relative to saline-treated SLE mice (1.09±0.06 vs. 1.37±0.06 and 0.36±0.04 vs. 0.55±0.10; all p<0.05), suggesting efficacy of the therapy. Mean arterial pressure (MAP; mmHg) was increased in SLE mice compared to controls (140±4 vs. 114±2; p<0.001). Nicotine prevented the rise in MAP in SLE mice (129±4; p=0.022), but not controls (121±3). This protection from hypertension coincided with a 46±5% lower renal cortical TNF-α in nicotine-treated SLE mice compared to saline-treated SLE mice (0.39±0.04 vs. 0.73±0.18), which is important because it has been previously shown that renal TNF-α plays a mechanistic role in the development of hypertension during SLE. Because nicotine acts on both ganglionic and peripheral cholinergic receptors, in a subsequent study mice were administered the selective α7nAChR agonist, PNU-282987 (0.38 mg/kg/day, IP), or vehicle for 28 days. PNU-282987-treated SLE mice had lower splenic protein expression of TNF-α and IL-6 relative to saline-treated SLE mice (0.33±0.01 vs. 0.54±0.03 and 0.40±0.08 vs. 0.86±0.05; all p<0.05). MAP was increased in SLE mice compared to controls (138±2 vs. 122±5). PNU-282987 prevented the rise in MAP in SLE mice (128±4), but not controls (125±5). These data suggest the anti-inflammatory effects of cholinergic agonists may protect from SLE hypertension and that the cholinergic anti-inflammatory pathway may be an important target in hypertensive patients with chronic inflammatory diseases.

scholarly journals The Anti-Inflammatory Effects of Angiogenin in an Endotoxin Induced Uveitis in Rats

2020 ◽  
Vol 21 (2) ◽  
pp. 413
Author(s):  
Jihae Park ◽  
Jee Taek Kim ◽  
Soo Jin Lee ◽  
Jae Chan Kim
Keyword(s):  
Western Blot ◽  
Inflammatory Cytokines ◽  
Aqueous Humor ◽  
Rat Model ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Ocular Tissue ◽  
Tnf Α ◽  
Anti Inflammatory

Angiogenin (ANG) is involved in the innate immune system and inflammatory disease. The aim of this study is to evaluate the anti-inflammatory effects of ANG in an endotoxin induced uveitis (EIU) rat model and the pathways involved. EIU rats were treated with balanced salt solution (BSS), a non-functional mutant ANG (mANG), or wild-type ANG (ANG). The integrity of the blood-aqueous barrier was evaluated by the infiltrating cell and protein concentrations in aqueous humor. Histopathology, Western blot, and real-time qRT-PCR of aqueous humor and ocular tissue were performed to analyze inflammatory cytokines and transcription factors. EIU treated with ANG had decreased inflammatory cells and protein concentrations in the anterior chamber. Compared to BSS and mANG, ANG treatment showed reduced expression of IL-1β, IL-8, TNF-α, and Myd88, while the expression of IL-4 and IL-10 was increased. Western blot of ANG treatment showed decreased expression of IL-6, inducible nitric oxide synthase (iNOS), IL-1β, TNF-α, and phosphorylated NF-κB and increased expression of IL-10. In conclusion, ANG seems to reduce effectively immune mediated inflammation in the EIU rat model by reducing the expression of proinflammatory cytokines, while increasing the expression of anti-inflammatory cytokines through pathways related to NF-κB. Therefore, ANG shows potential for effectively suppressing immune-inflammatory responses in vivo.

scholarly journals The inducing of caspase and bcl-2 pathway with royal jelly decreases the muscle tissue damage exposed with fluoride in rats

2021 ◽  
Author(s):  
Abdullah Aslan ◽  
Muhammed Ismail Can ◽  
Ozlem Gok ◽  
Seda Beyaz ◽  
Gozde Parlak ◽  
...  
Keyword(s):  
Protein Expression ◽  
Muscle Tissue ◽  
Caspase 3 ◽  
Royal Jelly ◽  
Female Rats ◽  
Standard Diet ◽  
Expression Levels ◽  
Group Standard ◽  
Tnf Α ◽  
Caspase 6

Abstract In this study, 42 Wistar albino female rats (n = 42, 8 weeks old) were used. Rats were divided into 6 groups and 7 rats included each group. Groups: (i) Control Group: Standard diet; (ii) RJ (royal jelly) Group: Standard diet + royal jelly; (iii) F50 Group: Standard diet + 50 mg/kg fluoride; (iv): F100 Group: Standard diet + 100 mg/kg fluoride; (v) F50 + RJ Group: Standard diet + 50 mg/kg fluoride + royal jelly; (iv): F100 + RJ Group: Standard diet + 100 mg/kg fluoride + royal jelly. After the 8-week study period, the rats were decapitated and their muscle tissues were removed. Expression levels of Caspase-3, Caspase-6, Bax, Tnf-α, IL1-α and Bcl-2 proteins in muscle tissue were determined by Western Blotting method. Histopathological analyzes were also performed on the muscle tissue. MDA, GSH, and CAT analyzes were determined by spectrophotometric analysis. According to our findings, Bcl-2, Tnf-α and IL1-α protein expression were increased in damage groups compared to control and royal jelly groups, Caspase-3, Caspase-6 and Bax protein expression levels decreased in damage groups. There was an increase in MDA level in damage groups compared to the control and royal jelly groups, CAT and GSH levels decreased in damage groups. According to histopathological analysis results, edema and inflammatory cell formations were found in the injury groups, a tendency to decrease in these injuries was observed in the treatment groups. Based on these results, we can say that royal jelly has protective effects against fluoride damage.

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