NUCLEAR MEDICINE AND BIOLOGY
·
2022
·
IF 2.947
Hongliang Wang,Liu Yang,Keyi Lu,Xiaoshan Guo,Rui Xi,Weixuan Dong,Kaixin Qin,Haiyan Liu,Hua Wei,Yan Cheng,Zhifang Wu,Sijin Li
Objective Given the limitation of biomarkers to predict the renal function progression in diabetic nephropathy , N-(6-[ 18 F]Fluoropyridin-3-yl)glycine (6-[ 18 F]FPyGly) was used to evaluate renal function progression in a rat model of diabetic nephropathy. Methods Twenty male Sprague-Dawley rats were randomly divided into four groups, including the healthy control group (HC group), diabetic nephropathy group (DNM group), routine diet treated diabetic nephropathy group (RDNM group), and high fat/high sucrose -diet-fed diabetic nephropathy group (HDNM group). All renal function parameters were determined from animal PET renograms . P and T max represent the curve peak counts and the time to the curve peak counts of 6-[ 18 F]FPyGly in kidneys after injection, C 1/2 and the 15 min/Peak ratio represent the time from peak to 1/2 peak in the clearance phase, and the ratio of the curve counts at 15 min to the curve peak counts. Results P, T max , C 1/2 , and 15 min/peak ratio of each rat were significantly correlated with S-Cr, BUN . There were significant differences in T max , P, serum creatinine (S Cr), and blood urea nitrogen (BUN) levels between HC and DNM groups. P and the 15 min/Peak ratio were significantly different among DNM, RDNM, and HDNM groups, while T max and C 1/2 were only significantly different between DNM and RDNM or HDNM groups. There only was a significant difference in BUN between the DNM and HDNM groups. Conclusion The renal function parameters P, T max , C 1/2 and 15 min/peak value obtained by dynamic renal imaging based on 6-[ 18 F]FPyGly could reflect changes of renal function in rats, which had a good correlation with S Cr and BUN, and showed more efficient in the diagnosis of diabetic nephropathy and renal function classification than S Cr and BUN.
研究领域:
医学影像
·
核医学
·
糖尿病
·
肾脏生理
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2018
·
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
·
食品科学
·
生物化学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CELL BIOCHEMISTRY AND BIOPHYSICS
·
2014
·Vol. 71
·期 2
·535-541
·
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
·
毒理学
·
肿瘤学
·
肾脏生理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Molecular Medicine Reports
·
2018
·Vol. 18
·期 6
·5445-5454
·
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
·
肾病学
·
神经病学
·
细胞生物学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Iranian Journal of Basic Medical Sciences
·
2022
·
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
·
毒理学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
RENAL FAILURE
·
2022
·
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
·
分子生物学
·
肾病学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
·
2017
·
IF 2.759
Yang Liu,Lei Wang,Yang Du,Zhiyuan Chen,Jia Guo,Xiaodong Weng,Xiao Wang,Min Wang,Danyang Chen,Xiuheng Liu
The aim of our study is to investigate the protective effect of apigenin and the role of the JAK2/STAT3 signaling pathway in renal ischemia/reperfusion injury (IRI) in rats. For in vivo experiments, rat kidneys were subjected to 45 min of ischemia , followed by 24 h of reperfusion. The kidneys were pretreated for 24 h with apigenin (4 mg/kg) intraperitoneally in the absence or presence of the JAK2 kinase-specific inhibitor AZD1480 (30 mg/kg). The serum creatinine and urea nitrogen levels were analyzed. Histologic examinations were evaluated. Expression of p-JAK2, p-STAT3, Bcl-2, Bax and Caspase-3 was detected by immunohistochemistry or western blot . For In vitro experiments, NRK-52E cells were exposed to I/R in the absence or presence of apigenin and JAK2 siRNA was used to explore JAK2/STAT3 activity. Cell viability , cell apoptosis and expression of p-JAK2, p-STAT3, Bcl-2, Bax and Caspase-3 were examined in NRK-52E culture after I/R. Consequently, apigenin conferred a renoprotective effect on the kidneys against IRI, as evidenced by decreased serum creatinine and urea nitrogen, mitigated renal histologic damage, improved NRK-52E cell viability and a decreased apoptotic index, including up-regulation of the anti-apoptotic protein Bcl-2 and down-regulation of the pro-apoptotic proteins Bax and Caspase3. However, AZD1480 and JAK2 siRNA blocked the apigenin-mediated renoprotective effects by attenuating the JAK2/STAT3 signaling pathway as well as abolished the effect of anti-oxidative stress and anti-apoptosis of apigenin. Our study demonstrates that apigenin pretreatment can protect against renal IRI via the activation of the JAK2/STAT3 signaling pathway.
研究领域:
药理学
·
肾病学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Bioengineered
·
2021
·
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
·
肾病学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FOOD RESEARCH INTERNATIONAL
·
2023
·
IF 8.1
Zhu Ying,Huang Yuyang,Li Meiying,Sun Bingyu,Liu Linlin,Lv Mingshou,Qu Min,Guan Huanan,Zhu Xiuqing
The high Fischer (F) ratio hemp peptide (HFHP) was prepared by enrichment using activated carbon adsorption, ultrafiltration, and Sephadex G-25 gel filtration chromatography. The OD 220 /OD 280 ratio reached 47.1 with a molecular weight distribution from 180 to 980 Da, a peptide yield up to 21.7 %, and the F value was 31.5. HFHP had high scavenging ability of DPPH, hydroxyl free radicals, and superoxide. Mice experiments showed that the HFHP increased the activity of superoxide dismutase and glutathione peroxidase. The HFHP had no effect on the body weight of mice, but prolonged their weight-bearing swimming time. The lactic acid, serum urea nitrogen, and malondialdehyde of the mice after swimming was reduced, and the liver glycogen increased. The correlation analysis indicated that the HFHP had significant anti-oxidation and anti-fatigue properties.
研究领域:
生物化学
·
药理学
·
营养学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Functional Foods
·
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
·
营养学
·
运动科学
✓ 已验证
产品关联
DOI
高影响因子
Journal of Natural Medicines
·
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
·
生物化学
·
分子生物学
·
医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
World Journal of Traditional Chinese Medicine
·
2024
·
IF 4.3
Gao Hong-Xue,Liu Zhi-Qiang,Hou Zong,Song Feng-Rui,Xing Jun-Peng,Zheng Zhong,Liu Shu
Objective: This study aimed to elucidate the active components and mechanisms of Plantago asiatica L. (PAL) in the treatment of gout. Materials and Methods: Based on its polarity, PAL was partitioned into three parts, P1, P2, and P3, through gradient elution using AB-8 macroporous resin columns. The primary constituents of these fractions include iridoids, phenylethanoid glucosides, and flavonoids. Subsequently, a comprehensive in vitro and in vivo screening and evaluation model was developed considering the fundamental pathological processes of gout, including the inhibition of uric acid (UA) production, augmentation of UA excretion, and anti-inflammatory effects. This model was used to analyze the anti-gout activity of P1, P2, P3, and the overall extracts derived from PAL. Results: All the PAL parts exhibited specific therapeutic properties as part of gout therapy. Specifically, the P2 part demonstrated the ability to diminish interleukin-1 beta levels, lower UA concentrations, suppress joint inflammation in rats, and restore abnormal parameters associated with gout, such as creatinine and urea nitrogen. These findings highlight the significant effect of P2 on gout treatment. Conclusions: Following a thorough assessment of the outcomes derived from diverse anti-gout experiments, P2 exhibited superior anti-gout properties compared to the remaining parts. P2 demonstrated a restorative effect on the aberrant parameters associated with gout, thereby comprehensively elucidating the therapeutic mechanism of P2 against gout. This study provides substantial evidence and serves as a reference for future investigations regarding the material foundation of PAL in gout treatment.
研究领域:
药理学
·
药用植物研究
·
生物化学
·
炎症研究
✓ 已验证
产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）