INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2018
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IF 3.909
Yujuan Li,Yizhou Xin,Fangxue Xu,Mengmeng Zheng,Xiaozhi Xi,Xiaowei Cui,Hui Cao,Hong Guo,Chunchao Han
The maca polysaccharides optimal extraction conditions were obtained by using response surface methodology (RSM) method and the anti-fatigue activity of maca polysaccharides (MCP) was explored. The maca polysaccharides extract yield of RSM could reach 9.97 mg/g by using the model predicts, and the total sugar and protein purity were 61.00% and 4.46% with the further isolation process, respectively. And the monosaccharide compositions obtained by gas chromatograph (GC) were composed of rhamnose (rha), glucose (glc), galactose (gal) with the ratio of 2.34:10.21:1.00. Furthermore, the anti-fatigue activity was evaluated by the swimming parameter, biochemistry parameters (liver glycogen (LG), blood urea nitrogen (BUN), and lactic acid (LD)), the result indicated that the low-dose maca polysaccharides group had the significant anti-fatigue activity.
研究领域:
药学
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食品科学
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生物化学
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DOI
PubMed
高影响因子
CELL BIOCHEMISTRY AND BIOPHYSICS
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2014
·Vol. 71
·期 2
·535-541
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IF 2.38
Lin Lin,Zheng Jing,Zhu Weiping,Jia Ning
Cisplatin-induced generation of reactive oxygen species leads to acute nephrotoxicity limiting its use in the treatment of various cancers. Gelsemine, an alkaloid isolated from Gelsemium elegans , is known to possess anti-inflammatory and anti-cancer activities. This study was aimed to investigate as to whether gelsemine can serve as a protective agent against cisplatin-induced nephrotoxicity. Male Wistar rats were divided into 6 groups, each with 6 rats. Group 1 served as control and received the vehicles (peanut oil for 14 days and 0.9 % saline on day 14 for gelsemine and cisplatin respectively). Group 2 received a single intraperitoneal injection of cisplatin on day 14. Group 3 and 4 were pretreated with two different doses of gelsemine in addition to cisplatin, and group 5 and 6 received only gelsemine. The effects of gelsemine on cisplatin-induced nephrotoxicity were examined by measuring anti-oxidant enzymes activities, lipid peroxidation, and DNA damage in the kidneys, a well-established model of oxidative damage. Pretreatment of rats with gelsemine caused a significant attenuation of cisplatin-induced DNA and oxidative damages. The blockade of lipid peroxidation and xanthine oxidase activity was accompanied by increased production and/or activity of anti-oxidants, both enzymatic (catalase, glutathione peroxidase, glutathione reductase, and glutathione- S -transferase) and non-enzymatic (GSH). The biomarkers of kidney malfunctioning, creatinine, and blood urea nitrogen were ameliorated. The results of the present study suggest that gelsemine effectively suppressed cisplatin-induced renal injury by improving redox status.
研究领域:
药理学
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毒理学
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肿瘤学
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肾脏生理学
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DOI
PubMed
高影响因子
Molecular Medicine Reports
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2018
·Vol. 18
·期 6
·5445-5454
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IF 1.922
Yang Su,Jingxiao Lu,Pian Gong,Xianguo Chen,Chaozhao Liang,Jie Zhang
Acute kidney injury (AKI) is a clinically common and severe complication of ischemia‑reperfusion (I/R), associated with high morbidity and mortality rates, and prolonged hospitalization. Rapamycin is a type of macrolide, primarily used for anti‑rejection therapy following organ transplantation and the treatment of autoimmune diseases. Rapamycin has been identified to exert a protective effect against AKI induced by renal I/R as an autophagy inducer. However, whether rapamycin preconditioning may relieve AKI following cerebral I/R (CIR) remains to be fully elucidated. The purpose of the present study was to investigate the effects of CIR on the renal system of rats and the role of rapamycin in AKI following CIR. In the present study, a CIR model was established in Sprague‑Dawley rats via a 90‑min period of middle cerebral artery occlusion and 24 h reperfusion, and pretreatment with an intraperitoneal injection of rapamycin (dosage: 1 mg/kg; 0.5 h) prior to CIR. The levels of serum creatinine and blood urea nitrogen (BUN), and the expression of inflammation‑, apoptosis‑ and autophagy‑associated markers were subsequently measured. In addition to certain histopathological alterations to the kidney, it was identified that CIR significantly increased the levels of serum creatinine, BUN, tumor necrosis factor‑α and interleukin‑1β, and significantly induced apoptosis and autophagy. It was observed that rapamycin induced autophagy through the mammalian target of rapamycin complex 1/autophagy‑related 13/unc‑51 like autophagy activating kinase 1 signaling pathway, and that rapamycin pre‑treatment significantly improved renal function and alleviated renal tissue inflammation and cell apoptosis in rats following CIR. In conclusion, the results suggested that rapamycin may alleviate AKI following CIR via the induction of autophagy.
研究领域:
药理学
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肾病学
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神经病学
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细胞生物学
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分子生物学
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DOI
PubMed
高影响因子
Journal of Functional Foods
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2018
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IF 3.47
Rui-dan Wang,Guan-hua Su,Lin Wang,Qing Xia,Rui Liu,Qun Lu,Jiu-liang Zhang
This study was aimed at evaluating the hypouricemic effect of rape bee pollen from Qinghai province in China. Rape bee pollen crude extracts (RPCE) was obtained by n-butanol extraction and purified by polyamide resin and AB-8 resin respectively to generate five fractions (fraction 1–5). In vitro , fraction 5 had strongest inhibition on xanthine oxidase (XO) (IC 50 = 0.21 ± 0.02 mg mL −1 ) among five fractions and had reversible and mixed inhibitory effect on XO. Fraction 5 was further purified and then generated fraction 5′. In vivo , fraction 5′ had lower serum UA level and could reduce serum BUN, Cr levels and hepatic XO activity more effectively than RPCE in potassium oxonate-induced hyperuricemic mice . Moreover, fraction 5′ had higher CAT activity and content of GSH in hyperuricemic mice. Six compounds including quercetin-3-O-(2″-O-glucopyranosyl)-glucopyranoside (peak 1), quercetin-3-O-(2″-O-glucopyranosyl)-rhamnopyranoside (peak 2), kaempferol-3-O-(2″-O-glucopyranosyl)-glucopyranoside (peak 3) and N′, N″-di- p -coumaroylspermidine (peak 4–6) in RPCE were identified by using HPLC-ESI-QTOF-MS/MS, whereas only peak 4 to 6 were found in fraction 5′. This study shows that rape bee pollen has potential clinical application value as an effective anti-hyperuricemia bioactive drug or functional food.
研究领域:
药理学
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生物化学
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食品科学
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医学
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产品关联
DOI
高影响因子
Iranian Journal of Basic Medical Sciences
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2022
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IF 2.532
Yan Wang,Yun-hui Zhang,Yin-ru Tang,Jie Lan,Zhi-ying Huang,Wei Tian,Qian Huang,Yan Peng,Yuan Gao,Yue-qin Hu,Xue-nong Zhang
Objective(s): Cisplatin (CDDP) is a highly effective chemotherapeutic agent, but its clinical application has been limited by nephrotoxicity. Tanshinone Ⅰ (T-I), a phenanthrenequinone compound extracted from the Chinese herb Danshen, has been used to improve circulation and treat cardiovascular diseases. The aim of this study was to investigate the protective effect of T-I on CDDP-induced nephrotoxicity in mice. Materials and Methods: The BALB/c mouse models of nephrotoxicity were established by a single intraperitoneal injection of 20 mg/kg CDDP on the first day of the experiment. Three hours prior to CDDP administration, the mice were dosed with 10 mg/kg and 30 mg/kg T-I for 3 consecutive days intraperitoneally to explore nephroprotection of T-I. Results: Treatment with T-I significantly reduced blood urea nitrogen and creatinine levels in serum observed in CDDP-administered mice, especially at a dose of 30 mg/kg. T-I at 30 mg/kg significantly decreased malondialdehyde levels and increased glutathione levels and the enzymatic activity of catalase in kidney tissue compared to CDDP. Additionally, T-I (30 mg/kg) significantly reversed the CDDP-decreased expression level of superoxide dismutase 2 protein in renal tissue. Histopathological evaluation of the kidneys further confirmed the protective effect of T-I. Conclusion: The findings of this study demonstrate that T-I can protect against CDDP-induced nephrotoxicity through suppression of oxidative stress.
研究领域:
药理学
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毒理学
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分子生物学
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DOI
PubMed
高影响因子
RENAL FAILURE
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2022
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IF 3.222
Qi Xiao
Background To prove the internal connection, we deciphered the effect of cinnamaldehyde on kidney senescence through establishing animal and cell models.Methods In vivo, a rat senescence model was constructed using D-galactose (D-gal), and the modeled rats were further treated with cinnamaldehyde. In vitro, rat renal tubular epithelial cells (NRK-52E) were transfected with miR-155 mimic or inhibitor and then treated with cinnamaldehyde, D-gal or PI3K inhibitor (LY294002). The serum levels of blood urea nitrogen (BUN) and serum creatinine (Scr) of the rats were measured by an automatic biochemical analyzer. Pathological changes of kidney were determined by hematoxylin-eosin staining. The senescence and viability of NRK-52E cells were assessed by SA-β-gal staining and CCK-8 assay, respectively. The levels of miR-155, p-PI3K/PI3K, p-Akt/Akt, LC3B (LC3-II and LC3-I) and Beclin1 were detected by qRT-PCR, immunohistochemistry, or western blot.Results D-gal elevated the levels of BUN, Scr and miR-155 in the kidney, induced the renal pathological damage, inhibited the cell viability, increased the numbers of SA-β-gal-, LC3B- and Beclin1-positive cells and upregulated the levels of LC3-II/LC3-I and Beclin1 both in the kidney and cells. Cinnamaldehyde reversed D-gal-induced effects on the kidney and cells, and moreover, the cinnamaldehyde-induced anti-D-gal effects on cells could be suppressed by miR-155 mimic but promoted by miR-155 inhibitor. LY294002 potentiated D-gal-induced effects, and reversed cinnamaldehyde- and miR-155 inhibitor-caused impacts on the PI3K/Akt pathway and LC3-II/LC3-I level in D-gal-induced cells.Conclusion Cinnamaldehyde attenuates kidney senescence and injury through PI3K/Akt pathway-mediated autophagy via downregulating miR-155.
研究领域:
药理学
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分子生物学
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肾病学
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细胞生物学
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DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
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2024
·
IF 13.3
Meng Li,Biwen Yang,Jiayi Tang,Mengling Ning,Zerong Guan,Zhenzhen Li,Binggang Ye,Huiqing Zhong,Zhouyi Guo,Zhiming Liu
Development of organelle-targeted fluorescent carbon dots (CDs) has attracted extensive attention recently, however, the application of CDs for monitoring cell membrane integrity is rarely reported. Herein, we propose a kind of amphiphilic CDs (∼2.84 nm) derived from o -phenylenediamine and urea (termed M-CDs). M-CDs display high-affinity capacity to polysaccharide structures, which allows the rapid (∼within 30 s), wash-free fluorescence (FL) imaging of microbes, including bacteria and fungi. For mammalian cells, M-CDs can selective bind to the intracellular cytoskeletal filaments when the cells undergo cytomembrane destruction. More interestingly, the FL feature of M-CDs is polarity-dependent that emits the maximum emission wavelength from 501 to 561 nm when the solvent polarity increases from 0.02 to 0.32, which offers the opportunity to detect the polarity microenvironment. We observe that the polarity increases significantly when M-CDs pass through the broken cytomembrane. M-CDs are finally adopted for the fast morphometric analysis of abnormal erythrocytes in haematuria, providing a novel avenue for the rapid test of membrane-related diseases.
研究领域:
生物医学工程
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细胞生物学
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材料科学
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医学诊断
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DOI
高影响因子
Bioengineered
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2021
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IF 3.269
Xia Zhao,Jing Wang,Liying Tang,Pei Li,Jing Ru,Yuzhi Bai
The study was designed to explore the effects of Withaferin A (WFA) on hyperuricemia-induced kidney injury and its action mechanism. Potassium oxonate (PO) was employed to establish the hyperuricemic mouse model. The pathological changes of renal tissue were evaluated by hematoxylin-eosin and masson trichrome staining. The levels of creatinine, blood urea nitrogen (BUN), uric acid (UA) and xanthine oxidase (XOD) were detected using corresponding commercial kits. Expressions of collagen-related and apoptosis-associated proteins in renal tissues were, respectively, evaluated by immunofluorescence and western blotting. Cell apoptosis was detected by TUNEL assay, and transporter expressions using western blotting. Followed by WFA, NRK-52E cells were treated with UA before evaluation of apoptosis and fibrosis. Results indicated that WFA ameliorated renal damage, improved kidney function, and decreased levels of creatinine, BUN, UA, and XOD in PO-induced hyperuricemic mice. Furthermore, WFA significantly prevented renal fibrosis and increased the expression of collagen-related proteins. Similarly, WFA markedly inhibited renal apoptosis, accompanied by changes of apoptosis-related proteins. Importantly, expression of transporters responsible for the secretion of organic anion transporter 1 (OAT1), OAT3, ATP-binding cassette subfamily G member 2 (ABCG2) was remarkably enhanced whereas that of urate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) was reduced in renal tissues of mice with hyperuricemia. In vitro study revealed that WFA notably ameliorated UA-induced cell fibrosis and apoptosis. Taken together, WFA improves kidney function by decreasing UA via regulation of XOD and transporter genes in renal tubular cells.
研究领域:
药理学
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肾病学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Journal of Functional Foods
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2020
·
IF 3.701
Peixin Wang,Hongliang Zeng,Shaoling Lin,Zhigang Zhang,Yi Zhang,Jiamiao Hu
Hairtail ( Trichiurus lepturus ) is a nutritious marine product that has attracted increasing attention due to its bioactive compounds. In this study, the anti-fatigue properties of hairtail hydrolysate were evaluated by exhaustive swimming experiments. Results indicate hairtail peptide supplementation increased the exhaustive weight-loaded swimming time. Furthermore, decreases in blood lactic acid (BLA), blood urea nitrogen (BUN), creatine kinase (CK), and malondialdehyde (MDA) content; and increases in glycogen content and antioxidant enzymes activities were observed in mice receiving hairtail peptides treatment after a 30 min swimming test. Pearson correlation analysis suggests fatigue indexes, including energy sources (hepatic glycogen and muscle glycogen content), metabolites (BLA and BUN content), and CK content significantly correlated with antioxidant levels (glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities and MDA content) and fecal SCFA content (propionic acid and butyrate acid content). In conclusion, long-term supplementation with hairtail peptides may improve exercise performance by relieving fatigue.
研究领域:
海洋生物学
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营养学
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运动科学
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DOI
高影响因子
Journal of Natural Medicines
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2020
·Vol. 75
·期 1
·129-141
·
IF 2.055
An Meng-Fei,Wang Ming-Yue,Shen Chang,Sun Ze-Rui,Zhao Yun-Li,Wang Xuan-Jun,Sheng Jun
Abstract Isoorientin (ISO), a natural flavonoid compound, has been identified in several plants and its biological activity is determined and the study on lowering uric acid has not been reported. In view of the current status of treatment of hyperuricemia, we evaluated the hypouricemic effects of ISO in vivo and in vitro, and explored the underlying mechanisms. Yeast extract-induced hyperuricemia animal model as well as hypoxanthine and xanthine oxidase (XOD) co-induced high uric acid L-O2 cell model and enzymatic experiments in vitro were selected. The XOD activity and uric acid (UA) level were inhibited after the treatment of ISO in vitro and in vivo. Furthermore, serum creatinine (CRE) and blood urea nitrogen (BUN) levels were also significantly reduced and liver damage was recovered in pathological histology after the ISO administration in hyperuricemia animal model. The results of mechanism illustrated that protein expressions such as XOD, toll-like receptor 4 (TLR4), cathepsin B (CTSB), NLRP3, and its downstream caspase-1 as well as interleukin-18 (IL-18) were markedly downregulated by ISO intervention in vitro and in vivo. Our results suggest that ISO exerts a urate-lowering effect through inhibiting XOD activity and regulating TLR4-NLRP3 inflammasome signal pathway, thus representing a promising candidate therapeutic agent for hyperuricemia. Graphic abstract Both animal models and in vitro experiments suggested that ISO may effectively lower uric acid produce. The mechanism might be the inhibition of XOD activity and NLRP3 inflammasome of upregulation.
研究领域:
药理学
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生物化学
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分子生物学
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医学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF PHARMACY AND PHARMACOLOGY
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2024
·
IF 2.8
Song Zeyu,Li Zhenyuan,Pan Tao,Liu Teng,Gong Baifang,Wang Zhixia,Liu Ke,Fan Huaying
ObjectivesAcute kidney injury (AKI) caused by cisplatin (CDDP) is a complex, critical illness with no effective or specific treatment. The purpose of the study was to assess the protective effect of protopanaxadiol (PPD) on the kidneys in CDDP-induced AKI models and its possible mechanisms.MethodsIn vitro, the protection of PPD was assessed in HK-2. KM mice were injected with CDDP to induce AKI models in vivo. The determination of blood urea nitrogen and serum creatinine (SCr) was performed, and pathological changes were examined by histopathological examination. Immunostaining and western blot analyses were used to analyze the expression levels of proteins.ResultsPPD can increase the viability of HK-2 cells damaged by CDDP, improve cell morphology, and alleviate the symptoms of AKI in mice. In addition, PPD can down-regulate the protein expression of TRF and up-regulate the protein expression of Ferritin heavy chain, Glutathione peroxidase 4, and ferroptosis suppressor protein 1 reduce the iron content in cells and kidney tissues, and restore the antioxidant defense system.ConclusionPPD has an inhibitory effect on cisplatin-induced nephrotoxicity, which may be related to the inhibition of ferroptosis by regulating iron metabolism and lipid peroxidation.
研究领域:
药理学
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肾病学
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细胞生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
TECHNOLOGY AND HEALTH CARE
·
2024
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IF 1.4
Jiang Yanan,Zhang Chengyi,Zhang Xinyue,Lan Na,Zhao Zihan,Xv Yawei,Wang Qi,Wang Siwei,Chen Baifeng,Chen Xi,Wang Yilin
BACKGROUND: In recent years, hyperuricemia and acute gouty arthritis have become increasingly common, posing a serious threat to public health. Current treatments primarily involve Western medicines with associated toxic side effects. OBJECTIVE: This study aims to investigate the therapeutic effects of total flavones from Prunus tomentosa (PTTF) on a rat model of gout and explore the mechanism of PTTF’s anti-gout action through the TLR4/NF- κ B signaling pathway. METHODS: We measured serum uric acid (UA), creatinine (Cr), blood urea nitrogen (BUN), tumor necrosis factor-alpha (TNF- α ), interleukin-1 beta (IL-1 β ), and interleukin-6 (IL-6) levels using an enzyme-linked immunosorbent assay (ELISA). Histopathological changes were observed using HE staining, and the expression levels of relevant proteins were detected through Western blotting. RESULTS: After PTTF treatment, all indicators improved significantly. PTTF reduced blood levels of UA, Cr, BUN, IL-1 β , IL-6, and TNF- α , and decreased ankle swelling. CONCLUSIONS: PTTF may have a therapeutic effect on animal models of hyperuricemia and acute gouty arthritis by reducing serum UA levels, improving ankle swelling, and inhibiting inflammation. The primary mechanism involves the regulation of the TLR4/NF- κ B signaling pathway to alleviate inflammation. Further research is needed to explore deeper mechanisms.
研究领域:
药理学
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免疫学
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风湿病学
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产品关联
DOI
PubMed
高影响因子
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