11 results on '"*APIGENIN"'
Search Results
2. Apigenin ameliorates doxorubicin-induced renal injury via inhibition of oxidative stress and inflammation
- Author
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Qijing Wu, Wei Li, Jing Zhao, Wei Sun, Qianqian Yang, Chong Chen, Ping Xia, Jingjing Zhu, Yiceng Zhou, Guoshun Huang, Chen Yong, Min Zheng, Enchao Zhou, and Kun Gao
- Subjects
Doxorubicin ,Nephrotoxicity ,Apigenin ,Oxidative stress ,Inflammation ,Mice ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Background and objective: Doxorubicin (DOX) is an anthracycline antitumor antibiotic widely utilized in treating various tumors. Nevertheless, the toxicity of DOX toward normal cells limits its applicability, with nephrotoxicity considered a major dose-limiting adverse effect. Apigenin (APG), a flavonoid widely distributed in natural plants, has been reported to have antioxidant, anti-inflammatory, and mild tumor-suppressive properties. In this study, we investigated the role of APG in DOX-induced nephrotoxicity and chemotherapeutic efficacy. Methods: Male BALB/c mice were administered DOX (11.5 mg/kg) via the tail vein to establish the DOX nephropathy model. After treatment with or without APG (125, 250, and 500 mg/kg) for two weeks, urine, serum, and tissue samples were collected to evaluate proteinuria, serum albumin, serum creatinine (Scr), blood urea nitrogen (BUN), superoxide dismutase (SOD) activity, malondialdehyde (MDA), glutathione (GSH), and pathological changes. Rat renal tubular epithelial cells (NRK52E), murine podocyte cells (MPC5), and murine breast cancer cells (4T1) were utilized to verify the effect of APG on DOX-induced cell injury. An MTT assay was employed to analyze cell viability. Apoptosis was evaluated using a colorimetric TUNEL staining and cleaved caspase-3 protein analysis by western blotting. A reactive oxygen species (ROS)/superoxide (O2-) fluorescence probe was employed to determine oxidative injury. Western blotting was used to analyze nephrin, α-smooth muscle actin (α-SMA), collagen I (Col1), fibronectin (FN), and SOD2 expression. The mRNA levels of tumor necrosis factor-α (TNF-α), interleukin-18 (IL-18), IL-6, NACHT, LRR, PYD domain-containing protein 3 (NLRP3), caspase-1, and IL-1β were tested by reverse transcription-polymerase chain reaction (RT-PCR). Results: APG ameliorated DOX-elicited renal injuries in both the glomeruli and tubules. The DOX + APG groups had much lower tissue MDA, IL-6, TNF-α, NLRP3, caspase-1, and IL-1β levels and generation of intracellular ROS, but significantly higher SOD activity and GSH levels compared to those of the DOX group. Additionally, APG attenuated DOX-induced morphological changes, loss of cellular viability, and apoptosis in NRK-52E and MPC-5 cells, but not in 4T1 cells. Conclusion: APG has a protective role against DOX-induced nephrotoxicity, without weakening DOX cytotoxicity in malignant tumors. Thus, APG may serve as a potential protective agent against renal injury and inflammatory diseases and may be a promising candidate to attenuate renal toxicity in cancer patients treated with DOX.
- Published
- 2021
- Full Text
- View/download PDF
3. Effect of apigenin, kaempferol and resveratrol on the gene expression and protein secretion of tumor necrosis factor alpha (TNF-α) and interleukin-10 (IL-10) in RAW-264.7 macrophages.
- Author
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Palacz-Wrobel, Marta, Borkowska, Paulina, Paul-Samojedny, Monika, Kowalczyk, Malgorzata, Fila-Danilow, Anna, Suchanek-Raif, Renata, and Kowalski, Jan
- Subjects
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APIGENIN , *RESVERATROL , *POLYPHENOLS , *GENE expression , *CANCER cell secretions , *TUMOR necrosis factors , *INTERLEUKIN-10 genetics , *MACROPHAGES , *THERAPEUTICS - Abstract
Polyphenols such as apigenin, kaempferol or resveratrol are typically found in plants, including fruits, vegetables, herbs and spices, which have a wide range of biological functions such as antioxidative, anti-inflammatory, vasodilative, anticoagulative and proapoptotic. Discovering such multifunctional compounds in widely consumed plant-based products – ones that both inhibit the release of TNF-α from tissue macrophages and at the same time enhance the secretion of IL-10 – would be an important signpost in the quest for effective pharmacological treatment of numerous diseases that have an inflammatory etiology. The aim of the study is to investigate the impact of biologically active polyphenols such as apigenin, resveratrol and kaempferol on gene expression and protein secretion of IL-10 and TNF-α in line RAW-264.7. Cells were cultured under standard conditions. IL-10 and TNF-α genes expression were examined using QRT-PCR and to assess cytokines concentration ELISA have been used. Apigenin, kaempferol and resveratrol at a dose 30 μM significantly decrease the TNF-α expression and secretion. Apigenin decrease the IL-10 expression and secretion. Furthermore, increase in IL-10 secretion after administration of kaempferol and resveratrol were observed. In the process of administration of tested compounds before LPS, which activate macrophages, decrease of TNF-α secretion after apigenin and kaempferol and increase of IL-10 secretion after resveratrol were observed. The results of present work indicate that 1) apigenin, resveratrol and kaempferol may reduce the intensity of inflammatory processes by inhibiting the secretion of proinflammatory cytokine TNF-α, and resveratrol and kaempferol additionally by increasing the secretion of anti-inflammatory cytokine IL-10 2) the studies indicate the potentially beneficial – anti-inflammatory – impact of diet rich in products including apigenin, resveratrol and kaempferol. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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4. Apigenin attenuates hippocampal oxidative events, inflammation and pathological alterations in rats fed high fat, fructose diet.
- Author
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Kalivarathan, Jagan, Chandrasekaran, Sathiya Priya, Kalaivanan, Kalpana, Ramachandran, Vidhya, and Carani Venkatraman, Anuradha
- Subjects
- *
APIGENIN , *INFLAMMATION , *HIGH-fat diet , *HIGH-carbohydrate diet , *LABORATORY rats - Abstract
High calorie diet promotes oxidative stress and chronic low grade inflammation that predispose to brain dysfunction and neurodegeneration. Hippocampus region of the brain has been shown to be particularly sensitive to high calorie diet. We hypothesize that apigenin (API), a flavonoid could attenuate hippocampal derangements induced by high fat-high fructose diet (HFFD). In this study, we investigated the effects of API on oxidative stress and inflammation in the hippocampus, and compared with those of sitagliptin (STG), a standard drug with neuroprotective properties. The markers of oxidative stress and inflammation were examined using biochemical assays, western blotting and immunohistochemistry techniques. HFFD-fed rats showed severe pathological alterations and API treatment rescued the hippocampus from the derangements. API significantly improved the antioxidant machinery, reduced ROS levels and prevented the activation of the stress kinases, inhibitor of kappa B kinase beta (IKKβ) and c-Jun NH2 terminal kinase (JNK), and the nuclear translocation and activation of nuclear factor kappa B (NF-κB). The plasma levels of inflammatory cytokines were also reduced. Our findings suggest that hippocampal derangements triggered by HFFD feeding were effectively curtailed by API. Suppression of oxidative stress, NF-κB activation and JNK phosphorylation in the hippocampus are the mechanisms by which API offers neuroprotection in this model. [ABSTRACT FROM AUTHOR]
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- 2017
- Full Text
- View/download PDF
5. Apigetrin treatment attenuates LPS-induced acute otitis media though suppressing inflammation and oxidative stress
- Author
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Li-Juan Xu, Ming Li, and Hao Guo
- Subjects
Lipopolysaccharides ,Male ,0301 basic medicine ,Lipopolysaccharide ,Anti-Inflammatory Agents ,Inflammation ,Acute otitis media ,RM1-950 ,Pharmacology ,medicine.disease_cause ,Superoxide dismutase ,Mice ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,Animals ,Humans ,Apigenin ,Apigetrin ,Cells, Cultured ,chemistry.chemical_classification ,Reactive oxygen species ,Dose-Response Relationship, Drug ,biology ,Inflammatory response ,General Medicine ,Mice, Inbred C57BL ,Vascular endothelial growth factor ,Otitis Media ,Treatment Outcome ,030104 developmental biology ,Otitis ,chemistry ,Oxidative stress ,030220 oncology & carcinogenesis ,TLR4 ,biology.protein ,Therapeutics. Pharmacology ,Inflammation Mediators ,medicine.symptom - Abstract
The natural course of otitis media in children is acute and self-limiting. Nevertheless, about 10-20% children could experience recurrent or persistent otitis media. Thus, finding effective candidate to prevent acute otitis media is urgently required. In our study, mouse acute otitis media model was constructed by lipopolysaccharide (LPS) injection into the middle ear of mice via the tympanic membrane. Apigetrin (APT) is a flavonoid isolated from various herbal medicines, possessing anti-inflammatory and anti-oxidative bioactivities. However, if APT could attenuate acute otitis media in LPS-induced animal models, little is to be known. Hematoxylin and eosin (H&E) staining suggested that APT treatment reduced LPS-induced higher mucosa thickness. LPS-triggered inflammatory response was also inhibited by APT, as evidenced by the down-regulated neutrophils and macrophages. Additionally, the reduced inflammatory factors, including interleukin-1β (IL-lβ), tumor necrosis factor α (TNF-α), IL-6 and vascular endothelial growth factor (VEGF) were observed in APT-treated mice with acute otitis media. The process was associated with the inhibition of toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) pathway, which was proved by the blockage of TLR4, MyD88, p-IKKα, p-IκBα, and p-NF-κB using western blot analysis. Moreover, the production of reactive oxygen species (ROS) caused by LPS was also reduced by APT through promoting anti-oxidants, involving superoxide dismutase (SOD) activity, heme oxygenase-1 (HO-1), NADP(H) quinone oxidoreductase 1 (NQO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) expressions. In contrast, high levels of MDA and kelch-like ECH-associated protein 1 (Keap 1) in LPS-treated mice were down-regulated by APT, which might be associated with the inactivation of NF-κB. In vitro, APT exhibited anti-inflammatory and anti-oxidant effects with little cytotoxicity in LPS-stimulated cells. Together, the data above indicated that APT could ameliorate acute otitis media through inhibiting inflammation and oxidative stress.
- Published
- 2019
6. Vitexin reverses the autophagy dysfunction to attenuate MCAO-induced cerebral ischemic stroke via mTOR/Ulk1 pathway
- Author
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Jin Jiang, Jingcun Dai, and Hong Cui
- Subjects
Male ,0301 basic medicine ,medicine.medical_treatment ,Vitexin ,Apoptosis ,Inflammation ,Pharmacology ,Brain Ischemia ,Nitric oxide ,Rats, Sprague-Dawley ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Autophagy ,medicine ,Animals ,Autophagy-Related Protein-1 Homolog ,cardiovascular diseases ,Apigenin ,Mechanistic target of rapamycin ,PI3K/AKT/mTOR pathway ,Sirolimus ,biology ,business.industry ,TOR Serine-Threonine Kinases ,Infarction, Middle Cerebral Artery ,General Medicine ,Rats ,Stroke ,Disease Models, Animal ,Oxidative Stress ,030104 developmental biology ,Cytokine ,chemistry ,biology.protein ,medicine.symptom ,business ,030217 neurology & neurosurgery - Abstract
Stroke, as a kind of acute cerebrovascular diseases, has greatly influenced the patients' quality of life and left a huge public health burden. Vitexin is a flavone C-glycoside (apigenin-8-C-?-D-glucopyranoside) present in several medicinal and other plants. This study aims to explore the role of vitexin in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic stroke. The results showed that the MCAO-induced brain infarction was obviously decreased by vitexin. And the abnormal protein levels of Caspase-3, Bcl-2-associated X protein (Bax), antigen identified by monoclonal antibody (Ki-67) and B cell lymphoma 2 (Bcl-2) in MCAO model rats were reversed by vitexin. Further research indicated that vitexin alleviated MCAO-induced oxidative injury by reducing the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA) and nitric Oxide (NO). In addition, vitexin attenuated the secretion of pro-inflammatory cytokine (interleukin (IL)-6 and tumor necrosis factor alpha (TNF-?)) and increased anti-inflammatory cytokine (IL-10) production to ameliorate MCAO-induced inflammation. What's more, vitexin repressed the MCAO-induced autophagy through mechanistic target of rapamycin (mTOR)/Ulk1 pathway. Specifically, the MCAO-induced decreased expression of mTOR, peroxisome proliferator-activated receptor ? (PPAR?) and p62 were inhibited by vitexin. At the same time, MCAO-induced increased expression of Ulk1, Beclin1 and rate of LC3?/LC3? also were repressed by vitexin. But the inhibition of vitexin on the MCAO-induced oxidative injury, apoptosis and inflammation were reversed by rapamycin. These results implied that vitexin suppressed the autophagy dysfunction to attenuate MCAO-induced cerebral ischemic stroke via mTOR/Ulk1 pathway.
- Published
- 2018
7. Effect of apigenin, kaempferol and resveratrol on the gene expression and protein secretion of tumor necrosis factor alpha (TNF-α) and interleukin-10 (IL-10) in RAW-264.7 macrophages
- Author
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Monika Paul-Samojedny, Malgorzata Kowalczyk, Anna Fila-Danilow, Renata Suchanek-Raif, Paulina Borkowska, Marta Palacz-Wrobel, and Jan Kowalski
- Subjects
Lipopolysaccharides ,0301 basic medicine ,medicine.medical_treatment ,Anti-Inflammatory Agents ,Gene Expression ,Pharmacology ,Resveratrol ,Cell Line ,Proinflammatory cytokine ,Mice ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Stilbenes ,medicine ,Animals ,Secretion ,Apigenin ,Kaempferols ,Inflammation ,Tumor Necrosis Factor-alpha ,Macrophages ,food and beverages ,General Medicine ,Interleukin-10 ,Interleukin 10 ,RAW 264.7 Cells ,030104 developmental biology ,Cytokine ,Biochemistry ,chemistry ,030220 oncology & carcinogenesis ,Cytokines ,Tumor necrosis factor alpha ,Kaempferol - Abstract
Polyphenols such as apigenin, kaempferol or resveratrol are typically found in plants, including fruits, vegetables, herbs and spices, which have a wide range of biological functions such as antioxidative, anti-inflammatory, vasodilative, anticoagulative and proapoptotic. Discovering such multifunctional compounds in widely consumed plant-based products – ones that both inhibit the release of TNF-α from tissue macrophages and at the same time enhance the secretion of IL-10 – would be an important signpost in the quest for effective pharmacological treatment of numerous diseases that have an inflammatory etiology. The aim of the study is to investigate the impact of biologically active polyphenols such as apigenin, resveratrol and kaempferol on gene expression and protein secretion of IL-10 and TNF-α in line RAW-264.7. Cells were cultured under standard conditions. IL-10 and TNF-α genes expression were examined using QRT-PCR and to assess cytokines concentration ELISA have been used. Apigenin, kaempferol and resveratrol at a dose 30 μM significantly decrease the TNF-α expression and secretion. Apigenin decrease the IL-10 expression and secretion. Furthermore, increase in IL-10 secretion after administration of kaempferol and resveratrol were observed. In the process of administration of tested compounds before LPS, which activate macrophages, decrease of TNF-α secretion after apigenin and kaempferol and increase of IL-10 secretion after resveratrol were observed. The results of present work indicate that 1) apigenin, resveratrol and kaempferol may reduce the intensity of inflammatory processes by inhibiting the secretion of proinflammatory cytokine TNF-α, and resveratrol and kaempferol additionally by increasing the secretion of anti-inflammatory cytokine IL-10 2) the studies indicate the potentially beneficial – anti-inflammatory – impact of diet rich in products including apigenin, resveratrol and kaempferol.
- Published
- 2017
8. Renoprotective effect of scutellarin on cisplatin-induced renal injury in mice: Impact on inflammation, apoptosis, and autophagy
- Author
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Ying Zhu, Liu-Mei Wu, Chao-Yue Sun, Juan Nie, Guangjuan Zheng, Zuo-Liang Zheng, Jie Zhao, Zu-Qing Su, and Bing Feng
- Subjects
Male ,0301 basic medicine ,p38 mitogen-activated protein kinases ,medicine.medical_treatment ,Glucuronates ,Inflammation ,Apoptosis ,RM1-950 ,Pharmacology ,Protective Agents ,Nephrotoxicity ,Mice ,Random Allocation ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,Autophagy ,Animals ,Apigenin ,Cisplatin ,Scutellarin ,business.industry ,General Medicine ,Acute Kidney Injury ,Mice, Inbred C57BL ,030104 developmental biology ,Cytokine ,chemistry ,030220 oncology & carcinogenesis ,Therapeutics. Pharmacology ,medicine.symptom ,business ,medicine.drug - Abstract
Cisplatin remains the standard first-line chemotherapeutic agent in the treatment of many types of cancers, but its clinical application is hindered by its severe nephrotoxicity. Previous studies reported that scutellarin enhanced the anti-cancer activity of cisplatin in lung cancer cells, with no confirmation on cisplatin-induced renal damage. Here, we investigated the nephroprotective effect of scutellarin on cisplatin-induced renal injury and its underlying mechanisms. Renal function, histological change, inflammation, apoptosis, autophagy and involved pathways were investigated. Pretreatment with scutellarin prevented cisplatin-induced decline of renal function including BUN, CRE, and histological damage. Scutellarin also reduced renal inflammation by suppressing the levels of pro-inflammatory cytokine, TNF-α and IL-6. Similarly, scutellarin administration inhibited apoptosis triggered by cisplatin through reducing the expressions of Cleaved caspase-3, Cleaved PARP, p53, and the ratio of Bax/Bcl-2. Moreover, scutellarin prevented cisplatin-induced inhibition of autophagy via enhancing LC3-II/LC3-I and Atg7, and inhibition of p62. Of note, the activations of JNK, ERK, p38 and stat3 induced by cisplatin were strikingly attenuated in scutellarin-treated mice. Thus, these results provide compelling evidence that scutellarin is a novel nephroprotectant against cisplatin-induced renal toxicity.
- Published
- 2019
9. Apigenin ameliorates doxorubicin-induced renal injury via inhibition of oxidative stress and inflammation.
- Author
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Wu, Qijing, Li, Wei, Zhao, Jing, Sun, Wei, Yang, Qianqian, Chen, Chong, Xia, Ping, Zhu, Jingjing, Zhou, Yiceng, Huang, Guoshun, Yong, Chen, Zheng, Min, Zhou, Enchao, and Gao, Kun
- Subjects
- *
APIGENIN , *OXIDATIVE stress , *PATHOLOGICAL physiology , *ANTINEOPLASTIC antibiotics , *RENAL tubular transport disorders , *SUPEROXIDES , *KIDNEY tubules , *URINE proteins - Abstract
DOX induces cytotoxicity in NRK-52E, MPC-5, and 4T1 cells, which is attenuated by APG in all cells except 4T1 cells. APG recovers the loss of SOD activity, GSH content, and the expression of WT-1 and nephrin. Furthermore, APG inhibits the genes involved in inflammatory and proteins related to fibrosis. These findings indicate a protective role of APG against DOX-induced nephrotoxicity dependent on suppression of oxidative stress and inflammatory response. APG, apigenin; DOX, doxorubicin; SOD, superoxide dismutase; GSH, glutathione, WT-1, Wilms tumor-1. [Display omitted] • Doxorubicin causes significant damage to both the glomeruli and tubules in kidney. • Apigenin ameliorates doxorubicin-induced renal injury via inhibition of oxidative stress and inflammation. • Apigenin protected renal cells against doxorubicin toxicity without reducing the sensitivity of tumor cells to doxorubicin. • Apigenin may serve as a promising protective agent against chemotherapy drug-induced renal toxicity in cancer patients. Doxorubicin (DOX) is an anthracycline antitumor antibiotic widely utilized in treating various tumors. Nevertheless, the toxicity of DOX toward normal cells limits its applicability, with nephrotoxicity considered a major dose-limiting adverse effect. Apigenin (APG), a flavonoid widely distributed in natural plants, has been reported to have antioxidant, anti-inflammatory, and mild tumor-suppressive properties. In this study, we investigated the role of APG in DOX-induced nephrotoxicity and chemotherapeutic efficacy. Male BALB/c mice were administered DOX (11.5 mg/kg) via the tail vein to establish the DOX nephropathy model. After treatment with or without APG (125, 250, and 500 mg/kg) for two weeks, urine, serum, and tissue samples were collected to evaluate proteinuria, serum albumin, serum creatinine (Scr), blood urea nitrogen (BUN), superoxide dismutase (SOD) activity, malondialdehyde (MDA), glutathione (GSH), and pathological changes. Rat renal tubular epithelial cells (NRK52E), murine podocyte cells (MPC5), and murine breast cancer cells (4T1) were utilized to verify the effect of APG on DOX-induced cell injury. An MTT assay was employed to analyze cell viability. Apoptosis was evaluated using a colorimetric TUNEL staining and cleaved caspase-3 protein analysis by western blotting. A reactive oxygen species (ROS)/superoxide (O 2 -) fluorescence probe was employed to determine oxidative injury. Western blotting was used to analyze nephrin, α-smooth muscle actin (α-SMA), collagen I (Col1), fibronectin (FN), and SOD2 expression. The mRNA levels of tumor necrosis factor-α (TNF-α), interleukin-18 (IL-18), IL-6, NACHT, LRR, PYD domain-containing protein 3 (NLRP3), caspase-1, and IL-1β were tested by reverse transcription-polymerase chain reaction (RT-PCR). APG ameliorated DOX-elicited renal injuries in both the glomeruli and tubules. The DOX + APG groups had much lower tissue MDA, IL-6, TNF-α, NLRP3, caspase-1, and IL-1β levels and generation of intracellular ROS, but significantly higher SOD activity and GSH levels compared to those of the DOX group. Additionally, APG attenuated DOX-induced morphological changes, loss of cellular viability, and apoptosis in NRK-52E and MPC-5 cells, but not in 4T1 cells. APG has a protective role against DOX-induced nephrotoxicity, without weakening DOX cytotoxicity in malignant tumors. Thus, APG may serve as a potential protective agent against renal injury and inflammatory diseases and may be a promising candidate to attenuate renal toxicity in cancer patients treated with DOX. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
10. Effect of vitexin on alleviating liver inflammation in a dextran sulfate sodium (DSS)-induced colitis model
- Author
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Shuni Duan, Jie Gao, Shuxian Chen, Song Huang, Xianhua Du, Ping Ding, Shaozhen Hou, and Jian Liang
- Subjects
Male ,0301 basic medicine ,Vitexin ,Inflammation ,RM1-950 ,Liver injury ,Pharmacology ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Western blot ,medicine ,Animals ,Apigenin ,Colitis ,Mice, Inbred BALB C ,medicine.diagnostic_test ,business.industry ,Dextran Sulfate ,NF-kappa B ,General Medicine ,medicine.disease ,Ulcerative colitis ,digestive system diseases ,Toll-Like Receptor 4 ,Disease Models, Animal ,030104 developmental biology ,Dextran ,Liver ,chemistry ,030220 oncology & carcinogenesis ,TLR4 ,Cytokines ,Therapeutics. Pharmacology ,Inflammation Mediators ,medicine.symptom ,business ,Signal Transduction - Abstract
As one of commonly used herbs with dual-purpose of drug and food, it has been reported that vitexin has hepatoprotective effects. However, the protective effects of vitexin on colitis-induced liver injury as well as the underlying molecular mechanisms remain unclear. The purpose of the current study was to investigate the effects and mechanisms of vitexin on liver injury induced by acute ulcerative colitis in mice. In this study, the mice model of acute ulcerative colitis was induced by 4 % dextran sodium sulphate (DSS). And then, the degree of liver injury in colitis mice was evaluated, the hepatic ALT, AST, TC and TG levels were measured by specific determination kits, the levels of TNF-α, IL-6 and IL-1β were examined by ELISA, the expressions of TLR4/NF-κB pathway related protein were detected by western blot analysis. The results indicated that hepatic histopathological changes induced by DSS were normalized by vitexin treatment, administration of vitexin decreased the liver levels of ALT and TC in mice with liver injury and reduced the release amounts of DSS-induced pro-inflammatory cytokines TNF-α, IL-6 and IL-1β. Furthermore, we found that vitexin inhibited the activation of TLR4/NF-κB signaling pathway induced by DSS. In conclusion, vitexin possess hepatoprotective activities against colitis-induced liver injury, it has potential application prospects in the treatment of liver injury induced by ulcerative colitis.
- Published
- 2020
11. Clerodendrum petasites S. Moore: The therapeutic potential of phytochemicals, hispidulin, vanillic acid, verbascoside, and apigenin
- Author
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Premrutai Thitilertdecha, Nattawat Onlamoon, James M. Brimson, and Tewin Tencomnao
- Subjects
0301 basic medicine ,Petasites ,Clerodendrum ,Phytochemicals ,RM1-950 ,Flavones ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Verbascoside ,Glucosides ,Phenols ,Vanillic acid ,Animals ,Humans ,Medicine ,Apigenin ,Cancer ,Inflammation ,Vanillic Acid ,Pharmacology ,chemistry.chemical_classification ,biology ,Traditional medicine ,Phenylpropanoid ,business.industry ,Medicinal plant ,General Medicine ,biology.organism_classification ,Osteolytic bone diseases ,030104 developmental biology ,chemistry ,030220 oncology & carcinogenesis ,Hispidulin ,Therapeutics. Pharmacology ,business ,Neurological diseases - Abstract
Clerodendrum petasites S. Moore has been prescribed in Thai traditional medicine for over 30 years for the treatment of ailments including asthma, inflammation, fever, cough, vomiting, and skin disorders. The phytochemicals from this plant have been identified as phenolic acids, flavones, flavone glycosides, glycosides, phenylpropanoid, and diterpenoid. The pharmacological activities both in vitro and in vivo have mostly been reported from crude extracts and not from pure compounds. This review, therefore, brings together information on the specific phytochemicals found in C. petasites in order to provide a guide to the natural bioactive compounds that are potentially used in medicines together with mechanisms underlying their pharmacological uses. All relevant information was searched for the terms of plant name, naturally-occurring compounds, and traditional uses from reliable databases, such as PubMed, Science Direct and Google Scholar, along with Thai traditional medicine textbooks. There was no specific timeline set for the search and this review selected to report only mechanisms studied by using standard compounds for their biological activities. Four dominant compounds comprising hispidulin, vanillic acid, verbascoside, and apigenin, have robust evidence to support their medical effects. Hispidulin was discovered to be possibly responsible for the treatment of cancer, osteolytic bone diseases, and neurological diseases. Other compounds were also found to tentatively support the uses in inflammation and neurological diseases. C. petasites extracts may provide an option as complimentary medicine, and or for the pharmacological development of new drugs derived from the phytochemicals found within.
- Published
- 2019
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