scholarly journals Luteolin Improves Cyclophosphamide-Induced Cystitis through TXNIP/NLRP3 and NF-κB Pathways

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Hengshuai Zhang ◽  
Jiang Zhao ◽  
Qudong Lu ◽  
Bishao Sun ◽  
Xin Liu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Hemorrhagic Cystitis ◽  
Antioxidant Properties ◽  
Tunel Staining ◽  
Sprague Dawley ◽  
Bladder Tissue ◽  
Acute Cystitis ◽  
Current Therapies ◽  
Anti Inflammatory ◽  
Commercial Kits

Hemorrhagic cystitis is an important complication of cyclophosphamide chemotherapy, and current therapies for the disease are limited. The natural flavonoid luteolin (LUT) has significant anti-inflammatory and antioxidant properties, but its protective effect on cyclophosphamide (CYP)-induced bladder toxicity has yet to be evaluated. This study aims to explore the protective effect of LUT on CYP-induced acute cystitis in rats. Female Sprague-Dawley rats were randomly assigned to the control (CON) group, CON + LUT group, CYP group, and CYP + LUT group. A single intraperitoneal injection of CYP was administered to establish an acute hemorrhagic cystitis model. HE staining was performed to detect the degree of bladder tissue damage, and TUNEL staining was performed to count apoptotic cells. Oxidative stress indicators were measured using commercial kits, and bladder surgery was performed to assess urinary function. The levels of inflammatory cytokines, apoptosis-related indicators, TXNIP/NLRP3 pathway, and NF-κB pathway were detected by western blot. We found that LUT treatment reduced bladder bleeding, congestion, and edema caused by CYP. Compared with the CYP + LUT group, the level of apoptosis was more highly expressed in the CYP group. We also found that caspase-3, caspase-8, and Bax were significantly upregulated and Bcl-2 was downregulated after LUT treatment. In addition, LUT inhibited the activation of NF-κB signal pathway in the rat bladder tissue after CYP exposure. LUT treatment can also reduce the NLRP3 inflammasome (NLRP3, ASC, and caspase-1) and TXNIP in the bladder. Finally, LUT can reduce the increase in the urination frequency and maximum urination pressure caused by cystitis. These results indicate that LUT displays effective anti-inflammatory, antioxidant, and antiapoptotic properties in CYP-induced acute hemorrhagic cystitis rats by inhibiting the TXNIP/NLRP3 and NF-κB pathways. LUT may be a potent therapeutic agent for the prevention and treatment of hemorrhagic cystitis.

Protective Effect of Calcium Dobesilate Administration Against Hepatorenal Damage Induced By CCL4 In Male Mice

2021 ◽  
Author(s):  
Elham Hakimizadeh ◽  
Ayat Kaeidi ◽  
Mohammadreza Rahmani ◽  
Mohammad Allahtavakoli ◽  
Jalal Hassanshahi
Keyword(s):  
Protective Effect ◽  
Antioxidant Properties ◽  
Group Versus ◽  
Histopathological Change ◽  
Renal Tissue ◽  
Protective Effects ◽  
Male Mice ◽  
Calcium Dobesilate ◽  
Liver And Kidney ◽  
Anti Inflammatory

Abstract Purpose: Calcium dobesilate (CaD) has antioxidant and anti-inflammatory properties. In this study, the protective effects of CaD against hepatorenal damage induced by CCL4 in male mice were evaluated. Methods: Thirty male mice randomly were divided into five groups: Control, CaD 100 mg/kg, CCL4, CCL4+CaD 50 mg/kg, and CCL4+CaD 100 mg/kg. Drugs were administered orally once a day for 4-weeks. The liver and kidney indices (serum creatinine, blood urine nitrogen, alanine aminotransferase and aspartate aminotransferase levels) were determined. Also, hepatic and renal tissue oxidant/antioxidant markers (glutathione peroxidase, malondialdehyde, total antioxidant capacity, and superoxide dismutase) were measured. Cleaved caspase-3, Bax, and Bcl-2 protein levels were measured by immunoblotting method. The liver and kidney histopathological changes were evaluated by H&E staining.Results: CCL4 induces significant oxidative stress in the kidney and liver that was concomitant with functional and histopathological abnormalities in these organs in the CCL4 group versus the control (P<0.05). CaD could significantly improve the histopathological change in the liver and kidney tissues of CCL4+CaD 100 mg/kg mice versus the CCL4 group (P<0.05). In addition, CaD attenuated apoptosis in the liver and kidney tissues (P<0.05).Conclusion: The protective effect of CaD may be related to its anti-inflammatory and antioxidant properties.

scholarly journals The anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on acrylamide-induced neurotoxicity in rats

2019 ◽  
Author(s):  
Jie Guo ◽  
Xiaolu Cao ◽  
Xianmin Hu ◽  
Shulan Li ◽  
Jun Wang
Keyword(s):  
Oxidative Stress ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Tunel Staining ◽  
High Dose ◽  
Sprague Dawley ◽  
Curcumin Treatment ◽  
Concurrent Administration ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Background: As a chemical extensively used in industrial areas as well as formed during heating of carbohydrate-rich food and tobacco, acrylamide (ACR) has been known as well-established neurotoxic pollutant. Although the precise mechanism is unclear, enhanced apoptosis, oxidative stress and inflammation have been demonstrated to contribute to the ACR-induced neurotoxicity. In this study, we assessed the possible anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin, the most active component in a popular spice known as turmeric, on the neurotoxicity caused by ACR in rats. Methods: Curcumin at the dose of 50 and 100 mg/kg was orally given to ACR- intoxicated Sprague-Dawley rats exposed by ACR at 40mg/kg for 4 weeks. All rats were subjected to behavioral analysis. The HE staining and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) staining were used to detect histopathological changes and apoptotic cells, respectively. The mRNA and protein expressions of apoptosis-related molecule telomerase reverse transcriptase (TERT) were detected using real-time PCR and immunohistochemistry, respectively. The contents of malondialdehyde (MDA) and glutathione (GSH) as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as the indicators for evaluating the level of oxidative stress in brain. The levels of pro-inflammatory cytokinestumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in cerebral homogenates were detected using ELISA assay. Results: Concurrent administration of curcumin at the oral doses of 50 and 100 mg/kg with ACR significantly protected the rats from ACR-induced weigh loss and motor function deficits, and improved the pathological alterations in the ACR-intoxicated brains. Curcumin treatment especially at a high dose enhanced the TERT mRNA expression level and increased the number of TERT-positive nerve cells in cortex tissues of ACR intoxicated rats. The levels of MDA, TNF-α and IL-1β in the cerebral homogenates were reduced, the contents of GSH as well as the activities of SOD and GSH-Px were increased by curcumin treatment, compared to ACR control group. Conclusions: These data suggested the anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on ACR-induced neurotoxicity in rats. And maintaining TERT-related anti-apoptotic function might be one mechanism underlying the protective effect of curcumin on ACR-intoxicated brains.

scholarly journals Intraperitoneal injection of ketamine enhances apoptosis in urothelium via autophagy in rats

2020 ◽  
Vol 18 ◽  
pp. 205873922093566
Author(s):  
Liqin Wei ◽  
Jitao Wu ◽  
Danxia Li ◽  
Zhengfei Shan
Keyword(s):  
Treatment Time ◽  
Control Group ◽  
Tunel Staining ◽  
High Dose ◽  
Sprague Dawley ◽  
Control Groups ◽  
Bladder Epithelium ◽  
Bladder Tissue ◽  
Expression Levels ◽  
Sprague Dawley Rats

Ketamine abusing is associated with ulcerative cystitis, but the mechanisms remain unclear. This study aimed to investigate the existence of ketamine-induced symptom in a rat model and evaluate the underlining mechanisms. Sprague-Dawley rats were chosen and randomly divided into 12 groups (n = 8), such as the control group, low dose of ketamine (10 mg/kg/day), middle dose of ketamine (30 mg/kg/day) and high dose of ketamine (50 mg/kg/day) groups. The experimental groups were administrated ketamine i.p. daily, whereas the control groups were administrated with saline. After 1, 3, and 6 months of treatment, the bladder tissues were collected. Haematoxylin and eosin (HE) staining and a transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay were used to evaluate the bladder epithelium pathology and urothelial apoptosis, respectively. The protein expression levels of LC3, p62, Beclin1 were assessed by Western blotting. HE staining results of the experimental rats showed the bladder tissue denudation of the urothelial epithelium with edema and congestion compared with the control groups. TUNEL staining showed a significantly higher number of apoptotic cells in experimental groups than in the control groups. The protein LC3 and Beclin1 had significantly higher levels compared with control groups. The protein p62 had lower levels compared with control groups. The expression levels correlated with contraction of ketamine and treatment time. HE staining, TUNEL staining and Western blot results showed dose-dependent, time-dependent autophage in ketamine-treated rats. All the results suggested that autophagy proteins might be involved in inflammatory response in rats.

Protective effect of N-acetylcysteine on experimental chronic cadmium nephrotoxicity in immature female rats

2009 ◽  
Vol 28 (4) ◽  
pp. 221-229 ◽  
Author(s):  
L Wang ◽  
D Chen ◽  
J Cao ◽  
Z Liu
Keyword(s):  
Protective Effect ◽  
Antioxidant Properties ◽  
Female Rats ◽  
Tubular Damage ◽  
Sprague Dawley ◽  
Tubular Necrosis ◽  
Sprague Dawley Rats ◽  
Nonenzymatic Antioxidants ◽  
Renal Tubular ◽  
Enzyme Markers

In the present study, female Sprague-Dawley rats received CdCl2 (50 mg/L through drinking water) and/or N-acetylcysteine (NAC, 120 mg/kg/day, orally) to investigate the protective effect of NAC on Cd-induced renal damage. Renal toxicity was evaluated by measuring the contents of total protein, β2-microglobulin, and α1-microglobulin in the urine and urinary enzyme markers of tubular necrosis, as well as levels of serum urea nitrogen and serum creatinine. Activities of antioxidant enzymes and contents of glutathione, malondialdehyde, and trace elements in the kidney were also measured. Animals that received both Cd and NAC showed a better renal function than those receiving Cd alone. In addition, NAC significantly reduced the levels of lipid peroxidation (LPO) in the kidney of cadmium-treated rats. The enzymic and nonenzymatic antioxidants levels are not restored, but their further decrease is prevented by NAC. Also NAC administration does not modify the urinary excretion of cadmium or contents of cadmium in the serum and kidney. In conclusion, NAC exerts its protective effect by decreased LPO and improving antioxidants status to prevent renal tubular damage induced by chronic Cd administration, most probably through its antioxidant properties.

scholarly journals The anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on acrylamide-induced neurotoxicity in rats

2020 ◽  
Author(s):  
Jie Guo ◽  
Xiaolu Cao ◽  
Xianmin Hu ◽  
Shulan Li ◽  
Jun Wang
Keyword(s):  
Oxidative Stress ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Acrylamide (ACR) formed during heating of tobacco and carbohydrate-rich food as well as widely applied in industries has been known as a well-established neurotoxic pollutant. Although the precise mechanism is unclear, enhanced apoptosis, oxidative stress and inflammation have been demonstrated to contribute to the ACR-induced neurotoxicity. In this study, we assessed the possible anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin, the most active component in a popular spice known as turmeric, on the neurotoxicity caused by ACR in rats.Methods: Curcumin at the dose of 50 and 100 mg/kg was orally given to ACR- intoxicated Sprague-Dawley rats exposed by ACR at 40mg/kg for 4 weeks. All rats were subjected to behavioral analysis. The HE staining and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) staining were used to detect histopathological changes and apoptotic cells, respectively. The mRNA and protein expressions of apoptosis-related molecule telomerase reverse transcriptase (TERT) were detected using real-time PCR and immunohistochemistry, respectively. The contents of malondialdehyde (MDA) and glutathione (GSH) as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as the indicators for evaluating the level of oxidative stress in brain. The levels of pro-inflammatory cytokinestumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the cerebral homogenates were detected using ELISA assay.Results: ACR-induced weigh loss, deficits in motor function as well as pathological alterations in brains were significantly improved in rats administrated with 50 and 100 mg/kg curcumin. TUNEL-positive apoptotic cells in curcumin-treated ACR intoxicated brains were less than those in the ACR model group. Curcumin administration especially at the dose of 100 mg/kg upregulated the TERT mRNA expression and enhanced the number of TERT-positive cells in ACR-intoxicated cortex tissues. Moreover, curcumin treatment reduced the concentrations of TNF-α, IL-1β and MDA, while increased the GSH contents as well as the SOD and GSH-Px activities in the cerebral homogenates, in comparison to ACR control group.Conclusions: These data suggested the anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on ACR-induced neurotoxicity in rats. Maintaining TERT-related anti-apoptotic function might be one mechanism underlying the protective effect of curcumin on ACR-intoxicated brains.

Protective effect of N-acetylcysteine on experimental chronic lead nephrotoxicity in immature female rats

2010 ◽  
Vol 29 (7) ◽  
pp. 581-591 ◽  
Author(s):  
Lin Wang ◽  
Zhenyong Wang ◽  
Jianzhu Liu
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
Female Rats ◽  
Tubular Damage ◽  
Enzymatic Antioxidants ◽  
Sprague Dawley ◽  
Renal Tubular ◽  
Enzyme Markers

Oxidative stress plays a key role in lead (Pb)-induced nephrotoxicity. N-acetylcysteine (NAC) is a potent oxygen free radicals scavenger and a metal chelator. In the present study, female Sprague-Dawley rats received PbAc2 (300 mg/L, via drinking water) and/or NAC (100 mg/kg/day, by intraperitoneal injection) to investigate the protective effect of NAC on Pb-induced renal damage and oxidative stress as well as its mechanism of action. Renal toxicity was evaluated by measuring urinary excretion of total protein, β2-microglobulin, albumin and urinary enzyme markers of tubular necrosis, as well as serum urea nitrogen level. Activities of antioxidant enzymes, contents of glutathione and malondialdehyde in kidney were also measured. Renal cell damage was assessed by electron microscopy. Animals that received both Pb and NAC showed a better renal function than those receiving Pb alone. Lead-induced tubular lesions and mitochondrial damage were markedly reduced in rats that also received NAC. Also, NAC significantly reduced the levels of lipid peroxidation and markedly restored the enzymic and non-enzymatic antioxidants levels in kidney of Pb-treated rats. Moreover, NAC administration significantly increased urinary Pb excretion and decreased its level in the serum and kidney. In conclusion, NAC treatment prevents renal tubular damage induced by chronic Pb administration, most probably through its antioxidant properties and chelating ability.

scholarly journals Los beneficios del consumo del cacao en la obesidad

UVserva ◽  
2018 ◽  
Author(s):  
José Ángel González Díaz
Keyword(s):  
Protective Effect ◽  
Antioxidant Properties ◽  
Noncommunicable Diseases ◽  
Predisposing Factor ◽  
Health Maintenance ◽  
Anti Inflammatory

Diversos estudios describen el efecto protector del consumo de cacao en el mantenimiento de la salud, asociando sus efectos con las propiedades antiinflamatorias y antioxidantes, recomendando su consumo en la prevención de enfermedades crónicas no transmisible. En México el incremento de la obesidad es alarmante, siendo un factor predisponente en el desarrollo de otras enfermedades crónicas no transmisibles. En este sentido, considerando que el padecer obesidad conlleva a la resistencia insulínica y al desarrollo de diabetes, la prioridad es buscar estrategias en la prevención o manejo de estas enfermedades en diferentes campos de investigación.Palabras Clave: Cacao; obesidad; pozol; diabetes; hipertensión AbstractSeveral studies describe the protective effect of cocoa consumption on health maintenance, associating its effects with anti-inflammatory and antioxidant properties, recommending its consumption in the prevention of chronic noncommunicable diseases. In Mexico the increase in obesity is alarming, being a predisposing factor in the development of other chronic non­communicable diseases. In this sense, considering that obesity leads insulinologic resistance and the development of diabetes, the priority is to seek strategies in the prevention or manage­ment of these diseases in different fields of investigation.Keywords: Cocoa; obesity; pozol; diabetes; hypertension

scholarly journals Alpha-Lipoic Acid Preconditioning and Ischaemic Postconditioning Synergistically Protect Rats from Cerebral Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/ NF-κB Signaling Pathway

2018 ◽  
Vol 51 (3) ◽  
pp. 1448-1460 ◽  
Author(s):  
Jing Zhang ◽  
Fan Xiao ◽  
Lieliang Zhang ◽  
Xifeng Wang ◽  
Xiaoyang Lai ◽  
...  
Keyword(s):  
Infarct Size ◽  
Signaling Pathway ◽  
Lipoic Acid ◽  
Neurological Deficit ◽  
Brain Oedema ◽  
Cerebral Injury ◽  
Tunel Staining ◽  
Alpha Lipoic Acid ◽  
Sprague Dawley ◽  
Anti Inflammatory

Background/Aims: A combination of alpha-lipoic acid preconditioning (ALAP) and ischaemic preconditioning (IPC) has not been tested in an in vivo rat cerebral ischaemia/reperfusion injury (I/RI) model, and the potential protective mechanisms have not been well elucidated. The aim of this study was to investigate the role of the TLR4/ MyD88/ NF-κB signaling pathway in the synergistically neuroprotective and anti-inflammatory effects of ALAP and IPC. Methods: One hundred and fifty male Sprague-Dawley rats, weighing 180-230 g, were randomly divided into the following 5 groups: 1) sham-operated control; 2) I/R; 3) I/R+ALAP; 4) I/R+IPC; 5) I/R+IPC+ALAP. After 2 h of reperfusion, the infarct size, neurological deficit scores, brain oedema, oxidative stress, and inflammatory and apoptotic biomarkers were assessed. In addition, reactive oxygen species (ROS) and cell apoptosis were detected by DHE staining and TUNEL staining, respectively. Results: Both ALAP and IPC treatment attenuated the I/RI-induced neuronal injury, reflected by reductions in the infarct size, neurological deficit scores, brain oedema, lactate dehydrogenase (LDH) release and the inflammatory response, as well as decreased HMGB1, TLR4, MyD88, p65, C-Caspase 3 and Bax expression and increased IKB-α, HO-1, SOD-2 and Bcl-2 expression compared to that in the I/R group. Furthermore, the combination of the two strategies had synergistic anti-inflammatory effects and antioxidant benefits, ultimately limiting neuronal apoptosis. Conclusion: The ‘cocktail’ strategy exhibited a significant neuroprotection against I/RI by attenuating neuroinflammation via inhibition of the TLR4/MyD88/NF-κB signaling pathway.

scholarly journals The anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on acrylamide-induced neurotoxicity in rats

2020 ◽  
Author(s):  
Jie Guo ◽  
Xiaolu Cao ◽  
Xianmin Hu ◽  
Shulan Li ◽  
Jun Wang
Keyword(s):  
Oxidative Stress ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Tunel Staining ◽  
High Dose ◽  
Sprague Dawley ◽  
Curcumin Treatment ◽  
Concurrent Administration ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Background: As a chemical extensively used in industrial areas as well as formed during heating of carbohydrate-rich food and tobacco, acrylamide (ACR) has been known as well-established neurotoxic pollutant. Although the precise mechanism is unclear, enhanced apoptosis, oxidative stress and inflammation have been demonstrated to contribute to the ACR-induced neurotoxicity. In this study, we assessed the possible anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin, the most active component in a popular spice known as turmeric, on the neurotoxicity caused by ACR in rats. Methods: Curcumin at the dose of 50 and 100 mg/kg was orally given to ACR- intoxicated Sprague-Dawley rats exposed by ACR at 40mg/kg for 4 weeks. All rats were subjected to behavioral analysis. The HE staining and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) staining were used to detect histopathological changes and apoptotic cells, respectively. The mRNA and protein expressions of apoptosis-related molecule telomerase reverse transcriptase (TERT) were detected using real-time PCR and immunohistochemistry, respectively. The contents of malondialdehyde (MDA) and glutathione (GSH) as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as the indicators for evaluating the level of oxidative stress in brain. The levels of pro-inflammatory cytokinestumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in cerebral homogenates were detected using ELISA assay. Results: Concurrent administration of curcumin at the oral doses of 50 and 100 mg/kg with ACR significantly protected the rats from ACR-induced weigh loss and motor function deficits, and improved the pathological alterations in the ACR-intoxicated brains. Curcumin treatment especially at a high dose enhanced the TERT mRNA expression level and increased the number of TERT-positive nerve cells in cortex tissues of ACR intoxicated rats. The levels of MDA, TNF-α and IL-1β in the cerebral homogenates were reduced, the contents of GSH as well as the activities of SOD and GSH-Px were increased by curcumin treatment, compared to ACR control group. Conclusions: These data suggested the anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on ACR-induced neurotoxicity in rats. And maintaining TERT-related anti-apoptotic function might be one mechanism underlying the protective effect of curcumin on ACR-intoxicated brains.

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