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Hydroalcoholic extract of Brazilian red propolis exerts protective effects on acetic acid-induced ulcerative colitis in a rodent model. Barbosa Bezerra Gislaine,de Menezes de Souza Luana,Dos Santos Adailma Santana,de Almeida Grace Kelly Melo,Souza Marília Trindade Santana,Santos Sandra Lauton,Aparecido Camargo Enilton,Dos Santos Lima Bruno,de Souza Araújo Adriano Antunes,Cardoso Juliana Cordeiro,Gomes Silvana Vieira Floresta,Gomes Margarete Zanardo,de Albuquerque Ricardo Luiz Cavalcanti Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Ulcerative colitis (UC) is a common intestinal inflammatory disease with an etiology that is not well understood. Although the anti-inflammatory and anti-oxidant effects of the hydroalcoholic extract of Brazilian red propolis (HERP) have been reported in various experimental models, its protective effect in models of UC have not been evaluated. The purpose of this study was to investigate the chemopreventive effect of hydroalcoholic extract of Brazilian red propolis (HERP) in acetic acid-induced colitis (AAIC) using a rodent model. The HERP was chemically characterised by HPLC/DAD analyses. Male rats were randomly assigned into four groups: sham, vehicle (with AAIC, treated with vehicle), P10 (with AAIC, treated with 10mg/kg HERP), and P100 (with AAIC, treated with 100mg/kg HERP). Treatments were performed for 7days, and colitis was induced on day seven. Animals were euthanized 24h after colitis induction and body weight, colon length, gross and histological scores, malondialdehyde (MDA) and myeloperoxidase (MPO) concentrations in colon tissue, and the immunohistochemical expression of inducible nitric oxide synthase (iNOS) were assessed. The major compounds found in HERP were liquiritigenin (68.8mg/g), formononetin (54.29mg/g), biochanin A (30.97mg/g), and daidzein (19.90mg/g). Rats treated with 10mg/kg HERP demonstrated significant decreases in MPO concentrations, gross and histological scores of tissue damage, and iNOS expression (p<0.05). Similarly, rats treated with 100mg/kg HERP demonstrated significant decreases in MPO levels (p<0.05) and histological scores of tissue damage (p<0.05). The results of this study indicate that oral administration of HERP attenuates AAIC in rats, which may be due to anti-inflammatory effects related to iNOS inhibition. 10.1016/j.biopha.2016.11.080
Hydroalcoholic extract of Araucaria sp. brown propolis alleviates ulcerative colitis induced by TNBS in rats by reducing inflammatory cell infiltration and oxidative damage. The Journal of pharmacy and pharmacology OBJECTIVE:To investigate the effects of Araucaria sp. brown propolis (ABP) against trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. METHODS:Animals received vehicle (1% DMSO, 1 ml/kg) or hydroalcoholic extract of ABP (hydroalcoholic extract of Araucaria sp. brown propolis (HEABP), 30, 100, and 300 mg/kg) orally, or dexamethasone (25 mg/kg, s.c.) for 5 days. On day 4, the animals received intracolonic TNBS (150 mg/kg), on day 6 they were euthanized. The weight of the animals, the macroscopic and microscopic colonic damage, reduced glutathione (GSH) and malondialdehyde (MDA) levels, and the activity of glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), and myeloperoxidase (MPO) were measured in colon homogenate. The action of HEABP and two isolated compounds in neutrophil migration was recorded. KEY FINDINGS:HEABP (100 and 300 mg/kg), but not dexamethasone, decreased colonic lesion, and increased colonic mucin staining. In parallel, HEABP decreased MDA and restored GSH levels and the activity of SOD, CAT, and GST in the colon. A dose-dependent inhibition of MPO activity was observed (LogIC50 = 1.9). Moreover, HEBPA and the junicedric and abietic acids inhibited the neutrophil chemotaxis in vitro and HEBPA reduced neutrophil migration in vivo. CONCLUSION:HEABP may be promising in the therapies for inflammatory bowel diseases, reducing oxidative and inflammatory damage, especially mediated by neutrophils. 10.1093/jpp/rgae083
Propolis Alleviates Acute Lung Injury Induced by Heat-Inactivated Methicillin-Resistant via Regulating Inflammatory Mediators, Gut Microbiota and Serum Metabolites. Nutrients Propolis has potential anti-inflammatory properties, but little is known about its efficacy against inflammatory reactions caused by drug-resistant bacteria, and the difference in efficacy between propolis and tree gum is also unclear. Here, an in vivo study was performed to study the effects of ethanol extract from poplar propolis (EEP) and poplar tree gum (EEG) against heat-inactivated methicillin-resistant (MRSA)-induced acute lung injury (ALI) in mice. Pre-treatment with EEP and EEG (100 mg/kg, ) resulted in significant protective effects on ALI in mice, and EEP exerted stronger activity to alleviate lung tissue lesions and ALI scores compared with that of EEG. Furthermore, EEP significantly suppressed the levels of pro-inflammatory mediators in the lung, including , , , and . Gut microbiota analysis revealed that both EEP and EEG could modulate the composition of the gut microbiota, enhance the abundance of beneficial microbiota and reduce the harmful ones, and partly restore the levels of short-chain fatty acids. EEP could modulate more serum metabolites and showed a more robust correlation between serum metabolites and gut microbiota. Overall, these results support the anti-inflammatory effects of propolis in the treatment of ALI, and the necessity of the quality control of propolis. 10.3390/nu16111598
Brazilian propolis extract reduces intestinal barrier defects and inflammation in a colitic mouse model. Shimizu Yuki,Suzuki Takuya Nutrition research (New York, N.Y.) Brazilian propolis is rich in cinnamic acid derivatives and reportedly reduces intestinal inflammation in rodents; however, the underlying mechanisms remain unclear. We hypothesized that the regulation of tight junction (TJ) barrier, Th17 cell differentiation, and/or, macrophage activation by cinnamic acid derivatives were involved in the propolis-mediated anti-inflammatory effect. Mice were orally administered 2% dextran sodium sulfate (DSS) in combination with either the feeding control or a diet containing 0.3% ethanol extract of Brazilian propolis for 9 days. DSS administration induced acute colitis in mice, whereas the propolis extract mitigated DSS-induced weight loss; colon shortening; increased plasma levels of lipopolysaccharide-binding protein; reduced expression of TJ proteins, such as zonula occludens, junctional adhesion molecule-A, occludin, and claudins; and increased expression of inflammatory cytokines, such as tumor necrosis factor (TNF) α, interleukin (IL) 6, and IL-17a. Cinnamic acid derivatives, such as artepillin C and caffeic acid phenethyl ester, present in the propolis extract suppressed the IL-17 production from cultured murine splenocytes through decreased retinoic acid-related orphan receptor gT expression. Baccharin, drupanin, and culifolin, which are also present in Brazilian propolis, reduced the TNF-α and/or IL-6 production by suppressing inflammatory signaling in murine RAW 264.7 macrophages. Taken together, the regulation of Th17 differentiation and macrophage activation by cinnamic acid derivatives, at least in part, contribute to the anti-inflammatory effect mediated by Brazilian propolis. 10.1016/j.nutres.2019.07.003
Oral administration of Korean propolis extract ameliorates DSS-induced colitis in BALB/c mice. Hwang Soonjae,Hwang Samnoh,Jo Minjeong,Lee Chang Gun,Rhee Ki-Jong International journal of medical sciences Inflammatory bowel disease (IBD) is a chronic disorder of the gastrointestinal tract characterized by inflammation. Although IBD is usually treated with anti-inflammatory agents, most of these treatments have limited efficacy. Propolis is a viscous mixture that honeybees produce by mixing saliva and honeycomb with exudate gathered from tree buds, sap flows, or other botanical sources. Although propolis has proved to ameliorate several inflammatory disorders, its therapeutic properties vary by geographical location, plant resources, bee species, and the solvents used in the extraction. In this study, we investigated the effects of Korean propolis in BALB/c mice with dextran sulfate sodium (DSS)-induced colitis. Korean propolis extract was diluted in drinking water, and the BALB/c mice were given DSS for 7 days and Korean propolis for 17 days. The mice were sacrificed on day 17. In the DSS-induced colitis model, Korean propolis significantly decreased the severity of colitis, as assessed by body weight, spleen weight, and colonic length. Furthermore, Korean propolis induced the reduction of the inflammatory cytokine KC, infiltration of immune cells, and colonic hyperplasia in mice with DSS-induced colitis. The Korean propolis also decreased the loss of goblet cells and antibody-reactivity to inflammatory markers in the colons of mice administered DSS. These results demonstrate for the first time that Korean propolis has an ameliorative effect on DSS-induced colonic inflammation in BALB/c mice. 10.7150/ijms.44834
Cardiorenal dysfunction and hypertrophy induced by renal artery occlusion are normalized by galangin treatment in rats. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Galangin is a polyphenolic compound found in Alpinia officinarum and propolis. This study investigated the effect of galangin on blood pressure, the renin angiotensin system (RAS), cardiac and kidney alterations and oxidative stress in two-kidney one-clipped (2K-1C) hypertensive rats. Hypertension was induced in male Sprague Dawley rats (180-220 g), and the rats were given galangin (30 and 60 mg/kg) and losartan (10 mg/kg) for 4 weeks (n = 8/group). Galangin decreased hypertension and cardiac dysfunction and hypertrophy, which was related to the reducing circulation angiotensin converting enzyme (ACE) activity and angiotensin II concentration (p < 0.05). These effects were consistent with the reduced overexpression of angiotensin II receptor type 1 (ATR), transforming growth factor beta 1 (TGF-β1) and collagen type I (Col I) protein in cardiac tissue (p < 0.05). Additionally, renal artery occlusion, procedure-induced kidney dysfunction and fibrosis were attenuated in the galangin-treated group. Galangin treatment normalized the overexpression of ATR and NADPH oxidase 4 (Nox-4) protein and normalized the downregulation of nuclear factor-erythroid Factor 2-related Factor 2 (Nrf-2) and haem oxygenase 1 (HO-1) in 2K-1C rats (p < 0.05). Galangin exhibited antioxidative effects, as it reduced systemic and tissue oxidative stress markers and increased catalase activity in 2K-1C rats (p < 0.05). In conclusion, galangin attenuated hypertension, renin-angiotensin system activation, cardiorenal damage and oxidative stress induced by renal artery stenosis in rats. These effects might be associated with modulation of the expression of ATR, TGF-β1 and Col I protein in the heart as well as ATR/Nox-4 and Nrf-2/HO-1 protein in renal tissue in hypertensive rats. 10.1016/j.biopha.2022.113231
Anti-Inflammatory and Anti-Hyperuricemic Effects of Chrysin on a High Fructose Corn Syrup-Induced Hyperuricemia Rat Model via the Amelioration of Urate Transporters and Inhibition of NLRP3 Inflammasome Signaling Pathway. Chang Yi-Hsien,Chiang Yi-Fen,Chen Hsin-Yuan,Huang Yun-Ju,Wang Kai-Lee,Hong Yong-Han,Ali Mohamed,Shieh Tzong-Ming,Hsia Shih-Min Antioxidants (Basel, Switzerland) Hyperuricemia is the main cause of gout and involved in the occurrence of many other diseases such as hyperlipidemia and hypertension correlated with metabolic disorders. Chrysin is a flavonoid compound found naturally in honey, propolis, and mushrooms and has anti-inflammatory and antioxidant effects. However, its mechanism of action is not clear yet. This study investigated the mechanism of chrysin's anti-hyperuricemic effect in hyperuricemia-induced rats fed with high-fructose corn syrup. Orally administrated chrysin for 28 consecutive days effectively decreased uric acid by inhibiting the activity of xanthine oxidase (XO) in the liver. Moreover, chrysin markedly downregulated the protein expression of uric acid transporter 1 (URAT1) and glucose transporter type 9 (GLUT9) and upregulated the protein expression of organic anion transporter 1 (OAT1) and human ATP-binding cassette subfamily G-2 (ABCG2). In addition, chrysin showed prominent anti-oxidative and inflammatory effects as the malondialdehyde (MDA) and interleukin 1 beta (IL-1β) concentration was reduced in both rat kidney and serum, which aligned with the inhibition of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling pathway activation. Collectively, our results strongly suggest that chrysin exhibits potent anti-hyperuricemic and anti-inflammatory effects that may yield new adjuvant treatments for gout. 10.3390/antiox10040564
Green propolis extract attenuates acute kidney injury and lung injury in a rat model of sepsis. Silveira Marcelo Augusto Duarte,Capcha José Manuel Condor,Sanches Talita Rojas,de Sousa Moreira Roberto,Garnica Margot S,Shimizu Maria Heloisa,Berretta Andresa,Teles Flávio,Noronha Irene L,Andrade Lúcia Scientific reports Sepsis is the leading cause of acute kidney injury (AKI) and lung injury worldwide. Despite therapeutic advances, sepsis continues to be associated with high mortality. Because Brazilian green propolis (GP) has promising anti-inflammatory, antioxidant, and immunomodulatory properties, we hypothesized that it would protect kidneys and lungs in rats induced to sepsis by cecal ligation and puncture (CLP). Male Wistar rats were divided into groups-control (sham-operated); CLP (CLP only); and CLP + GP (CLP and treatment with GP at 6 h thereafter)-all receiving volume expansion and antibiotic therapy at 6 h after the procedures. By 24 h after the procedures, treatment with GP improved survival, attenuated sepsis-induced AKI, and restored renal tubular function. Whole-blood levels of reduced glutathione were higher in the CLP + GP group. Sepsis upregulated the Toll-like receptor 4/nuclear factor-kappa B axis in lung and renal tissues, as well as increasing inflammatory cytokine levels and macrophage infiltration; all of those effects were attenuated by GP. Treatment with GP decreased the numbers of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling-positive cells in renal and lung tissue, as well as protecting the morphology of the renal mitochondria. Our data open the prospect for clinical trials of the use of GP in sepsis. 10.1038/s41598-021-85124-6
Flavonoid extract from propolis alleviates periodontitis by boosting periodontium regeneration and inflammation resolution via regulating TLR4/MyD88/NF-κB and RANK/NF-κB pathway. Journal of ethnopharmacology ETHNOPHARMACOLOGICAL RELEVANCE:In traditional Chinese medicine, propolis has been used for treating oral diseases for centuries, widely. Flavonoid extract is the main active ingredient in propolis, which has attracted extensive attention in recent years. AIM OF THE STUDY:The objective and novelty of the current study aims to identify the mechanism of total flavonoid extract of propolis (TFP) for the treatment of periodontitis, and evaluate the therapeutic effect of TFP-loaded liquid crystal hydrogel (TFP-LLC) in rats with periodontitis. METHODS:In this study, we used lipopolysaccharide-stimulated periodontal ligament stem cells (PDLSCs) to construct in vitro inflammation model, and investigated the anti-inflammatory effect of TFP by expression levels of inflammatory factors. Osteogenic differentiation was assessed using alkaline phosphatase activity and alizarin red staining. Meanwhile, the expression of toll like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor-kappa B (NF-κB), receptor activator of NF-κB (RANK) etc, were quantitated to investigate the therapeutic mechanism of TFP. Finally, we constructed TFP-LLC using a self-emulsification method and administered it to rats with periodontitis via periodontal pocket injection to evaluate the therapeutic effects. The therapeutic index, microcomputed tomography (Micro-CT), H&E staining, TRAP staining, and Masson staining were used for this evaluation. RESULTS:TFP reduced the expression of TLR4, MyD88, NF-κB and inflammatory factor in lipopolysaccharide-stimulated PDLSCs. Meanwhile, TFP simultaneously regulating alkaline phosphatase, RANK, runt-associated transcription factor-2 and matrix metalloproteinase production to accelerate osteogenic differentiation and collagen secretion. In addition, TFP-LLC can stably anchor to the periodontal lesion site and sustainably release TFP. After four weeks of treatment with TFP-LLC, we observed a decrease in the levels of NF-κB and interleukin-1β (IL-1β) in the periodontal tissues of rats, as well as a significant reduction in inflammation in HE staining. Similarly, Micro CT results showed that TFP-LLC could significantly inhibit alveolar bone resorption, increase bone mineral density (BMD) and reduce trabecular bone space (Tb.Sp) in rats with periodontitis. CONCLUSION:Collectively, we have firstly verified the therapeutic effects and mechanisms of TFP in PDLSCs for periodontitis treatment. Our results indicate that TFP perform anti-inflammatory and tissue repair activities through TLR4/MyD88/NF-κB and RANK/NF-κB pathways in PDLSCs. Meanwhile, for the first time, we employed LLC delivery system to load TFP for periodontitis treatment. The results showed that TFP-LLC could be effectively retained in the periodontal pocket and exerted a crucial role in inflammation resolution and periodontal tissue regeneration. 10.1016/j.jep.2023.117324