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#33639173   2021/02/24 To Up

Diphenyl diselenide ameliorates diabetic nephropathy in streptozotocin-induced diabetic rats via suppressing oxidative stress and inflammation.

Oxidative stress and inflammation are implicated in the occurrence and progression of diabetic nephropathy (DN). Diphenyl diselenide (DPDS) is a stable and simple diaryl diselenide with anti-hyperglycemic, anti-inflammatory, and antioxidant activities. However, the effects of DPDS on DN are still unclear to date. Herein, we aimed to explore whether DPDS could improve renal dysfunction in streptozotocin (STZ)-induced diabetic rats and its underlying mechanisms. STZ-induced DN rats were administered with DPDS (5 or 15 mg/kg) or metformin (200 mg/kg) once daily by intragastric gavage for 12 weeks. DPDS supplementation significantly improved hyperglycemia, glucose intolerance, dyslipidemia, and the renal pathological abnormalities, concurrent with significantly reduced serum levels of creatinine, urea nitrogen, urine volume, and urinary levels of micro-albumin, β2-microglobulin and N-acetyl-glucosaminidase activities. Moreover, DPDS effectively promoted the activities of antioxidant enzymes, and reduced the levels of MDA and pro-inflammatory factors in serum and the kidney. Furthermore, DPDS supplementation activated the renal Nrf2/Keap1 signaling pathway, but attenuated the high phosphorylation levels of NFκB, JNK, p38 and ERK1/2. Altogether, the current study indicated for the first time that DPDS ameliorated STZ-induced renal dysfunction in rats, and its mechanism of action may be attributable to suppressing oxidative stress via activating the renal Nrf2/Keap1 signaling pathway and mitigating inflammation by suppressing the renal NFκB/MAPK signaling pathways, suggesting a potential therapeutic approach for DN.
Xing Wang, Caina Li, Yi Huan, Hui Cao, Sujuan Sun, Lei Lei, Quan Liu, Shuainan Liu, Wenming Ji, Kaixun Huang, Zhufang Shen, Jun Zhou

1293 related Products with: Diphenyl diselenide ameliorates diabetic nephropathy in streptozotocin-induced diabetic rats via suppressing oxidative stress and inflammation.

8 Sample Kit50 ul4 Arrays/Slide4 Membranes/Box1ml4 Sample Kit5ug96T16 Arrays/Slide1-8 Sample Kit100 Tests / Kit2ug

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#33625930   2021/02/24 To Up

Kaempferol attenuates diabetic nephropathy in streptozotocin-induced diabetic rats by a hypoglycaemic effect and concomitant activation of the Nrf-2/Ho-1/antioxidants axis.

This study examined the protective effect of Kaempferol against streptozotocin-induced diabetic nephropathy (DN) in rats and studies the underlying mechanisms. Rats were divided into 4 groups as control, control + Kaempferol, STZ, and STZ + Kaempferol. All treatments were conducted for 8 weeks daily after the induction of diabetes. Kaempferol prevented STZ-induced weight and food loss and attenuated renal damage and the alterations in all biochemical related parameters. Concomitantly, Kaempferol reduced renal levels of TNF-α and IL-6, cleaved caspase-3, p38, and Bax, suppressing JNK phosphorylation and NF-κB p65 transactivation, and upregulation of Bcl-2. In both control and STZ-diabetic rats, Kaempferol reduced fasting glucose levels, increased fasting insulin levels and HOMA-β, reduced the levels of ROS and MDA, stimulated SOD and GSH levels, and increased the expression of Nrf2 and HO-1. In conclusion, Kaempferol prevents STZ-induced diabetic nephropathy, mainly, by antioxidant potential, mediated by the upregulation of the Nrf-2/HO-1 axis.
Ali S Alshehri

2670 related Products with: Kaempferol attenuates diabetic nephropathy in streptozotocin-induced diabetic rats by a hypoglycaemic effect and concomitant activation of the Nrf-2/Ho-1/antioxidants axis.

100ug100ug50 ul125 Bags/Unit2 mg100μg

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#33288293   2020/11/20 To Up

The herbicide dinitramine affects the proliferation of murine testicular cells via endoplasmic reticulum stress-induced calcium dysregulation.

The hazardous effects of herbicides are well known; however, their effects on the reproductive system remain unclear. In this study, we demonstrated the anti-proliferative effects of dinitramine (DN) on immature murine testicular cell lines (Leydig and Sertoli cells) mediated via endoplasmic reticulum (ER) stress-induced calcium dysregulation in the cytosol and mitochondria. The results demonstrated that the viability and proliferation of DN-treated TM3 and TM4 cells decreased significantly, even in the spheroid state. DN induced the apoptosis of TM3 and TM4 cells and decreased the expression of genes related to cell cycle progression. Treatment with DN increased the cytosolic and intramitochondrial levels of calcium by activating ER stress signals. DN activated the Erk/P38/Jnk Mapk pathway and inactivated the Pi3k/Akt pathway in murine testicular cells. Co-treatment with 2-aminoethoxydiphenyl borate (2-APB) mitigated DN-induced calcium upregulation in both testicular cell lines. Although 2-APB did not antagonize the anti-proliferative effect of DN in TM3 cells, treatment with 2-APB and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid restored the proliferation of DN-treated TM4 cells.
Jiyeon Ham, Sunwoo Park, Whasun Lim, Gwonhwa Song

2528 related Products with: The herbicide dinitramine affects the proliferation of murine testicular cells via endoplasmic reticulum stress-induced calcium dysregulation.

100ul105 x 50 ug100 ug/vial0.25 mL100 IU0.1 mg

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#33152427   2020/11/02 To Up

Huangkui capsule in combination with metformin ameliorates diabetic nephropathy via the Klotho/TGF-β1/p38MAPK signaling pathway.

Huangkui capsule (HKC), extracted from Abelmoschus manihot (L.) medic (AM), as a patent proprietary Chinese medicine on the market for approximately 20 years, has been clinically used to treat chronic glomerulonephritis. Renal fibrosis has been implicated in the onset and development of diabetic nephropathy (DN). However, the potential application of HKC for preventing DN has not been evaluated.
Li-Yuan Gu, Yun-Sun, Hai-Tao Tang, Zheng-Xin Xu

1607 related Products with: Huangkui capsule in combination with metformin ameliorates diabetic nephropathy via the Klotho/TGF-β1/p38MAPK signaling pathway.

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#33088425   2020/10/06 To Up

The pro-apoptotic actions of 2-methoxyestradiol against ovarian cancer involve catalytic activation of PKCδ signaling.

2-methoxyestradiol (2MeOE) is a natural metabolite of estradiol, which is generated by the action of CYP1A1 enzyme in the liver. We have previously shown that a flaxseed-supplemented diet decreases both the incidence and severity of ovarian cancer in laying hens, also induces CYP1A1 expression in liver. Recently, we have shown that as a biologically derived active component of flax diet, 2MeOE induces apoptosis in ovarian cancer cells which is partially dependent on p38 MAPK. The objective of this study was to elucidate the molecular mechanism of actions of 2MeOE, a known microtubule disrupting agent, in inducing apoptosis in ovarian tumors.
Purab Pal, Karen Hales, Dale Buchanan Hales

2564 related Products with: The pro-apoptotic actions of 2-methoxyestradiol against ovarian cancer involve catalytic activation of PKCδ signaling.

6 ml Ready-to-use 5 GEach

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#32948825   2020/09/18 To Up

Activation of GPR120 in podocytes ameliorates kidney fibrosis and inflammation in diabetic nephropathy.

Diabetic nephropathy (DN) is one of the most common causes of end-stage renal disease worldwide. ω3-Fatty acids (ω3FAs) were found to attenuate kidney inflammation, glomerulosclerosis, and albuminuria in experimental and clinical studies of DN. As G protein-coupled receptor 120 (GPR120) was firstly identified as the receptor of ω3FAs, we here investigated the function of GPR120 in DN. We first examined the renal biopsies of DN patients, and found that GPR120 expression was negatively correlated with the progression of DN. Immunofluorescence staining analysis revealed that GPR120 protein was mainly located in the podocytes of the glomerulus. A potent and selective GPR120 agonist TUG-891 (35 mg · kg · d, ig) was administered to db/db mice for 4 weeks. We showed that TUG-891 administration significantly improved urinary albumin excretion, protected against podocyte injury, and reduced collagen deposition in the glomerulus. In db/db mice, TUG-891 administration significantly inhibited the mRNA and protein expression of fibronectin, collagen IV, α-SMA, TGF-β1, and IL-6, and downregulated the phosphorylation of Smad3 and STAT3 to alleviate glomerulosclerosis. Similar results were observed in high-glucose-treated MPC5 podocytes in the presence of TUG-891 (10 μM). Furthermore, we showed that TUG-891 effectively upregulated GPR120 expression, and suppressed TAK1-binding protein-1 expression as well as the phosphorylation of TAK1, IKKβ, NF-κB p65, JNK, and p38 MAPK in db/db mice and high-glucose-treated MPC5 podocytes. Knockdown of GPR120 in MPC5 podocytes caused the opposite effects of TUG-891. In summary, our results highlight that activation of GPR120 in podocytes ameliorates renal inflammation and fibrosis to protect against DN.
Tian-Tian Wei, Le-Tian Yang, Fan Guo, Si-Bei Tao, Lu Cheng, Rong-Shuang Huang, Liang Ma, Ping Fu

1142 related Products with: Activation of GPR120 in podocytes ameliorates kidney fibrosis and inflammation in diabetic nephropathy.

16-22 Sample Kit100 μg4 Membranes/Box8 Sample Kit16 Arrays/Slide

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#32417374   2020/05/15 To Up

Hirudin reduces nephropathy microangiopathy in STZ-induced diabetes rats by inhibiting endothelial cell migration and angiogenesis.

Kidney is the most common location of microangiopathy in diabetic patients, and we designed this study to investigate the effects of hirudin on renal microangiopathy in STZ-induced diabetes rats and in vitro.
Xinxin Pang, Yage Zhang, Zining Peng, Xiujie Shi, Jiarui Han, Yufeng Xing

2212 related Products with: Hirudin reduces nephropathy microangiopathy in STZ-induced diabetes rats by inhibiting endothelial cell migration and angiogenesis.

96 tests1 mg1.00 flask1.00 flask400 ug1.00 flask96 assays400 ug1.00 flask1 mg1.00 flask1.00 flask

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#32405507   2020/04/29 To Up

Umbilical Cord-Derived Mesenchymal Stem Cells Ameliorate Nephrocyte Injury and Proteinuria in a Diabetic Nephropathy Rat Model.

Mesenchymal stem cells (MSCs) are shown to alleviate renal injury of diabetic nephropathy (DN) in rats. However, the underlying mechanism of this beneficial effect is not fully understood. The aims of this study are to evaluate effects of umbilical cord-derived mesenchymal stem cells (UC-MSCs) on renal cell apoptosis in streptozotocin- (STZ-) induced diabetic rats and explore the underlying mechanisms. Characteristics of UC-MSCs were identified by flow cytometry and differentiation capability. Six weeks after DN induction by STZ injection in Sprague-Dawley rats, the DN rats received UC-MSCs once a week for consecutive two weeks. DN-related physical and biochemical parameters were measured at 2 weeks after UC-MSC infusion. Renal histological changes were also assessed. Moreover, the apoptosis of renal cells and expression of apoptosis-related proteins were evaluated. Compared with DN rats, rats treated with UC-MSCs showed suppressed increase in 24-hour urinary total protein, urinary albumin to creatinine ratio, serum creatinine, and blood urea nitrogen. UC-MSC treatment ameliorated pathological abnormalities in the kidney of DN rats as evidenced by H&E, PAS, and Masson Trichrome staining. Furthermore, UC-MSC treatment reduced apoptosis of renal cells in DN rats. UC-MSCs promoted expression of antiapoptosis protein Bcl-xl and suppressed expression of high mobility group protein B1 (HMGB1) in the kidney of DN rats. Most importantly, UC-MSCs suppressed upregulation of thioredoxin-interacting protein (TXNIP), downregulation of thioredoxin 1 (TRX1), and activation of apoptosis signal-regulating kinase 1 (ASK1) and P38 MAPK in the kidney of DN rats. Our results suggest that UC-MSCs could alleviate nephrocyte injury and albuminuria of DN rats through their antiapoptotic property. The protective effects of UC-MSCs may be mediated by inhibiting TXNIP upregulation in part.
Lian Chen, E Xiang, Changyong Li, Bing Han, Quan Zhang, Wei Rao, Cuihong Xiao, Dongcheng Wu

1727 related Products with: Umbilical Cord-Derived Mesenchymal Stem Cells Ameliorate Nephrocyte Injury and Proteinuria in a Diabetic Nephropathy Rat Model.

24 wells1 mg1.00 flask18 kgs96 tests1.00 flask5 x 10A5 cells/vial 100 UG2 ml100 µg1 mg

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#32398108   2020/05/12 To Up

Kidney-targeted baicalin-lysozyme conjugate ameliorates renal fibrosis in rats with diabetic nephropathy induced by streptozotocin.

Diabetic nephropathy (DN) is one of the most common and serious complications of diabetes, and is the most important cause of death for diabetic patients. Baicalin (BAI) has anti-oxidative, anti-inflammatory and anti-apoptotic activities, which play a role in attenuating insulin resistance and protecting the kidney. Moreover, cell-specific targeting of renal tubular cells is an approach to enhance drug accumulation in the kidney.
Xiao-Peng Zheng, Qing Nie, Jing Feng, Xiao-Yan Fan, Yue-Lei Jin, Guang Chen, Ji-Wei Du

1776 related Products with: Kidney-targeted baicalin-lysozyme conjugate ameliorates renal fibrosis in rats with diabetic nephropathy induced by streptozotocin.

100ug100ug100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

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