Protective Effect Of Luteolin Research Articles

Protective effect of luteolin on indomethacin-induced gastric ulcer in rats

Protective effect of luteolin on indomethacin-induced gastric ulcer in rats

Protective Effects of Luteolin and Gallic Acid Against Storage-Induced Oxidative Damage in Whole Blood of Female Wistar Rats

Introduction: Whole blood undergoes oxidative stress that precipitates biochemical changes that can lead to lesions during storage. This study attempts to evaluate the effectiveness of gallic acid and luteolin separately and in their combined state against oxidative damage during blood storage. Materials and Methods: Rats were grouped into control and experimental. Blood collected was stored for 28 days at 4°C. On day 0, 14, and 28, blood was withdrawn to study oxidative stress markers, antioxidant enzymes, and protein oxidation products. Results: Catalase activity reduced in all groups. Thiobarbituric acid reactive substance (TBARS) level increased in control without antioxidants (p < 0.05). Combined antioxidants or when separately added at lower concentrations, significantly reduced the TBARS level. Individual antioxidants at higher concentrations increased TBARS as compared with control (p < 0.05; p < 0.01). Decrease in superoxide dismutase activity observed in control was prevented by the antioxidants. Protein sulfhydryl level was restored and sustained until the last day of storage in groups that received individual antioxidants at both concentrations and the combined form at a lower concentration. Addition of either luteolin or gallic acid and their combined form reduced advanced oxidation protein products formation noticed in the control during storage. Conclusions: Luteolin and gallic acid were beneficial in the area of increased antioxidant capacity, prevention of protein product formation, and maintenance of sulfhydryl level. Their combination also showed a synergistic effect that offered a potential to improve long-term storage of whole blood. The antioxidants could possibly collaborate to be excellent potential blood storage additives providing protection against oxidative damage through their antiradical properties.

Luteolin ameliorates LPS-induced acute liver injury by inhibiting TXNIP-NLRP3 inflammasome in mice

BackgroundChemical liver injury is one of the main causes of acute liver failure and death. To date, however, treatment strategies for acute liver injury have been limited. Therefore, there is an urgent need to find new therapeutic targets and effective drugs. NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome is a complex of multiple proteins that has been shown to induce cell death under inflammatory and stress pathologic conditions and is thought to provide new targets for the treatment of a variety of diseases. PurposeThe purpose of this study was to investigate whether luteolin has a protective effect on the liver and further elucidate whether it is realized through the thioredoxin interacting protein (TXNIP)-NLRP3 axis. Study designAcute hepatic injury in mice caused by intraperitoneal injection of lipopolysaccharide (LPS) was treated with or without luteolin. MethodsMale C57BL/6 mice and mouse primary hepatocytes were selected. TXNIP protein knockdown was achieved by siRNA, qPCR and Western blot were performed to explore the mechanism of luteolin in alleviating acute liver injury. ResultsThe results indicated that luteolin had a markedly protective effect on acute liver injury induced by LPS in mice by inhibiting the TXNIP-NLRP3 axis. Luteolin inhibits NLRP3 inflammasome activation by suppressing TXNIP, apoptosis associated speck-like protein containing a CARD domain (ASC), caspase-1, interleukin-1β (IL-1β) and IL-18 to reduce liver injury. In addition, luteolin inhibits LPS-induced liver inflammation by inhibiting the production of inflammation-related gene tumor necrosis factor-α (TNF-α), IL-10, and IL-6. What's more, luteolin alleviated LPS-induced hepatocyte injury by inhibiting oxidative stress and regulating MDA, SOD, and GSH levels. However, the protective effect of luteolin on acute LPS-induced liver injury in mice was blocked by si-TXNIP in vitro. ConclusionsThese combined data showed that luteolin may alleviate LPS-induced liver injury through the TXNIP-NLPR3 axis, providing new therapeutic targets and therapeutic drugs for subsequent studies.

Protective effect of Luteolin on atopic dermatitis murine model via IgE mediated immune response

Abstract Atopic dermatitis (AD) is a serious inflammatory condition associated with severe itching and persistent eczematous lesion. Therefore, the present study was intended to scrutinize the beneficial effect of Luteolin (LT) on the atopic dermatitis murine model. The effect of LT was investigated on the various parameters, such as oxidative stress and inflammation after induction of AD. The serum level of IgE, and cells of the WBC family (neutrophils, basophils, eosinophils, monocytes, lymphocytes, and total WBC) and histopathological analysis of skin tissue were also examined to confirm the effect of LT. Results of the study suggested that LT significantly inhibited the elevated IgE level together with improvement in injured skin tissue architecture. It also reduces oxidative stress (MDA, SOD, and GSH) and inflammation (IL-1β, IL-6, TNF-α, IFN-γ, IL-4, and IL-17A) as evidenced by ELISA analysis. The level of examined WBC family cells was found reduced significantly as compared to the AD model group. In western blot analysis, LT showed significant down-regulation of NF-ĸB and TLR-4. Collectively, our results suggest that LT can effectively reverse the effect of atopic dermatitis via improving immunological response.

Protective effects of luteolin on the venous endothelium.

Luteolin is a flavonoid with antioxidant properties already demonstrated in studies related to inflammation, tumor, and cardiovascular processes; however, there are no available information regarding its antioxidant effects at the venous endothelial site. We investigated the effects of luteolin (10, 20, and 50μmol/L) in cultures of rat venous endothelial cells. Nitric oxide (NO) and reactive oxygen species (ROS) were analyzed by fluorimetry; 3-nitrotyrosine (3-NT) residues were evaluated by immunofluorescence, and prostacyclin (PGI2) release was investigated by colorimetry. Intracellular NO levels were significantly enhanced after 10min of luteolin incubation, with a parallel decrease in ROS generation. These results were accompanied by a significant reduction in the expression of 3-NT residues and enhanced PGI2 rates. Therefore, luteolin is effective in reducing ROS thereby improving NO availability in venous endothelial cells. Besides, luteolin-induced decrease in 3-NT residues may correlate with the enhancement in endothelial PGI2 bioavailability. These findings suggest the future application of this flavonoid as a protective agent by improving endothelial function in several circulatory disorders related to venous insufficiency.

Protective effect of luteolin on acute lung injury in a rat model of sepsis

ABSTRACT We investigated the effects of luteolin (LUT) treatment on acute lung injury caused by cecal ligation and puncture (CLP) induced septic rats. We also investigated the relation between LUT and the cytokines, interleukin-10 (IL-10) and tumor necrosis factor-α (TNF-α). LUT was administered 1 h after CLP surgery. Administration of LUT reduced the glutathione level and superoxide dismutase activity in rat lung tissues. We also found significant reduction of malondialdehyde following LUT treatment. LUT administration also reduced TNF-α and IL-10 mRNA expression in lung tissue. Histopathologic investigation of lung tissue supported our biochemical and molecular findings. Administration of LUT ameliorated lung injury in CLP induced septic rats owing to its antioxidant and anti-inflammatory properties.

Effect of Luteolin on Biochemical, Immunohistochemical, and Morphometrical Changes in Rat Spinal Cord following Exposure to a 900 MHz Electromagnetic Field

ObjectiveThis study aimed to investigate the effect of exposure to a 900 MHz electromagnetic field (EMF) on the cervical spinal cord (CSC) of rats and the possible protective effect of luteolin (LUT) against CSC tissue damage. MethodsQuantitative data were obtained via stereological, biochemical, immunohistochemical, and histopathological techniques. We investigated morphometric value, superoxide dismutase (SOD) level, and the expression of high-mobility group box 1 protein molecules, as well as histological changes. ResultsThe total number of motor neurons in the EMF group significantly decreased in comparison with that in the control group (P < 0.05). In the EMF + LUT group, we found a significant increase in the total number of motor neurons compared with that in the EMF group (P < 0.05). SOD enzyme activity in the EMF group significantly increased in comparison with that in the control group (P < 0.05). By contrast, the EMF+LUT group exhibited a decrease in SOD level compared with the EMF group (P < 0.05). ConclusionOur results suggested that exposure to EMF could be deleterious to CSC tissues. Furthermore, the protective efficacy of LUT against SC damage might have resulted from the alleviation of oxidative stress caused by EMF.

Luteolin Attenuates Glycerol-Induced Acute Renal Failure and Cardiac Complications Through Modulation of Kim-1/NF-κB/Nrf2 Signaling Pathways

Acute renal failure (ARF) has been documented as a life-threatening disease with high morbidity and mortality. We investigated the protective effect of Luteolin against ARF. In this study, forty-male Wistar albino rats were randomly divided into four groups (n = 10). Group A received normal saline. Group B received glycerol (10 ml/kg BW, 50% v/v in sterile saline, i.m.). Groups C and D were pretreated with Luteolin 100 and 200 mg/kg for 7 days, and thereafter administered Glycerol (10 ml/kg BW, 50% v/v in sterile saline, i.m.). Administration of glycerol significantly increased systolic blood pressure, diastolic blood pressure and mean arterial pressure. Renal protein carbonyl and xanthine oxidase increased significantly while significant reduction in the activity of renal glutathione peroxidase, glutathione S-transferase and glutathione reductase was observed in the glycerol intoxicated rats. Furthermore, administration of glycerol led to significant increases in serum creatinine and blood urea nitrogen together with reduction in nitric oxide (NO) bioavailability. Immunohistochemistry revealed that glycerol intoxication enhanced expressions of kidney injury molecule 1, nuclear factor kappa beta and cardiac troponin (CTnI). However, Luteolin pretreatment normalized blood pressure, reduced markers of oxidative stress, renal damage, and improved NO bioavailability. Luteolin also downregulated the expressions of kidney injury molecule 1, nuclear factor kappa beta and cardiac troponin. Together, Luteolin might open a novel therapeutic window for the treatment of acute renal failure and cardiac complication.

The Protective Effect of Luteolin in Glucocorticoid-Induced Osteonecrosis of the Femoral Head.

Glucocorticoid-induced osteonecrosis of the femoral head (GIONFH) is a frequently occurring type of nontraumatic osteonecrosis. A failure of the timely treatment can eventually result in the collapse of the subchondral bone structure. Luteolin (Lut), a compound extracted from Rhizoma Drynariae, is reported to possess multiple pharmacological properties including anticancer, antioxidant, antiapoptosis, and antiinflammatory properties. However, whether Lut has a protective effect on the development of GIONFH remains unclear. In this study, we evaluated the effect of Lut on Dexamethasone (Dex)-induced STAT1/caspase3 pathway in vitro and evaluated GIONFH model in vivo. In vitro, Lut inhibited the upregulation of Dex-induced phospho-STAT1, cleaved caspase9, and cleaved caspase3. In addition, Lut inhibited Dex-induced expression of Bax and cytochrome c and increased the expression of B cell lymphoma-2(Bcl-2). In vivo, Lut decreased the proportion of empty lacunae in rats with GIONFH. Taken together, these findings indicate that Lut may have therapeutic potential in the treatment of GIONFH. Further, this effect might be achieved by suppressing mitochondrial apoptosis of osteoblasts via inhibition of STAT1 activity.

Canine atopic dermatitis: Role of luteolin as new natural treatment.

BackgroundLuteolin has been demonstrated to possess numerous biological effects. However, the effect of luteolin on LPS (Lipopolysaccharides) stimulation in CPEK cells has not been investigated.Hypothesis/ObjectivesAn in vitro model of atopic canine dermatitis was used to identify the antioxidant effect of luteolin as a new treatment that is capable of improving the conditions of veterinary patients.MethodsCPEK cells were treated with or without luteolin in the presence or absence of LPS. A cell viability assay was performed to test luteolin toxicity and the protective effect of luteolin after LPS stimulation. Additionally, enzyme‐linked immunosorbent assay (ELISA) kits were used to detect the levels of IL‐33, IL‐1β, IL‐6, and IL‐8.ResultsLuteolin was capable to significantly decrease levels expression of IL‐33, IL 1β, IL‐6, and IL‐8.Conclusions and clinical importanceLuteolin could be a new pharmacological treatment for canine atopic dermatitis.

Protective effects of luteolin on nephrotoxicity induced by long-term hyperglycaemia in rats.

ObjectiveThis study aimed to investigate whether luteolin delays the progress of diabetic nephropathy (DN) induced by streptozotocin.MethodsFifty-three healthy, 8-week-old, male Sprague–Dawley rats were randomly divided into the control (n = 6), model (n = 23), and experimental groups (n = 24). The rat model of diabetic nephropathy was established by intraperitoneal injection of streptozotocin. Rats in the experimental group were administered luteolin suspension of 80 mg/kg daily for 8 weeks. Blood glucose levels and body weight were recorded until the fourth week. After intragastric administration, blood flow and the protective effect of luteolin on diabetic nephropathy were evaluated.ResultsThe degree of renal apoptosis and fibrosis in the experimental group was milder, and glomerular structure was more complete compared with the model group. Nphs2 staining suggested that luteolin delayed apoptosis and deletion and fusion of podocytes under high glucose levels, and protected the filtration function of the basement membrane by upregulating Nphs2 protein expression. Time intensity curve results suggested that luteolin delayed deterioration of renal haemodynamics under hyperglycaemia.ConclusionsThis study shows that luteolin delays progression of diabetic nephropathy. This drug has potential wide applicability in future clinical application.

Luteolin attenuates sepsis‑induced myocardialinjury by enhancing autophagy in mice.

Sepsis-induced cardiomyopathy (SIC) is a complication of severe sepsis and septic shock characterized by an invertible myocardial depression. This study sought to explore the potential effects and mechanism of luteolin, a flavonoid polyphenolic compound, in lipopolysaccharide (LPS)-induced myocardial injury. Experimental mice were randomly allocated into 3 groups (25 mice in each group): The control group (NC), the LPS group (LPS) and the LPS + luteolin group (LPS + Lut). Before the SIC model was induced, luteolin was dissolved in DMSO and injected intraperitoneally for 10 days into LPS + Lut group mice. NC group and LPS group mice received an equal volume of DMSO for 10 days. On day 11, the animal model of sepsis-induced cardiac dysfunction was induced by intraperitoneal injection of LPS. A total of 12 h after LPS injection, measurements and comparisons were made among the groups. Luteolin administration improved cardiac function, attenuated the inflammatory response, alleviated mitochondrial injury, decreased oxidative stress, inhibited cardiac apoptosis and enhanced autophagy. In addition, luteolin significantly decreased the phosphorylation of AMP-activated protein kinase (AMPK) in septic heart tissue. The protective effect of luteolin was abolished by 3-methyladenine (an autophagy inhibitor) and dorsomorphin (compound C, an AMPK inhibitor), as evidenced by decreased autophagic activity, destabilized mitochondrial membrane potential and increased apoptosis in LPS-treated cardiomyocytes, but was mimicked by 5-aminoimidazole-4-carboxamide ribonucleotide (an AMPK activator), suggesting that luteolin attenuates LPS-induced myocardial injury by increasing autophagy through AMPK activation. Luteolin may be a promising therapeutic agent for treating SIC.

Luteolin Attenuates Atherosclerosis Via Modulating Signal Transducer And Activator Of Transcription 3-Mediated Inflammatory Response.

BackgroundInflammatory factors play a crucial role throughout the development and progression of atherosclerosis, which has been considered as a chronic vascular inflammatory disease. Luteolin, a natural flavonoid which exists in many natural medicinal materials, has anti-inflammatory, anti-fibrotic and other pharmacological effects. Recently, the protective effects of luteolin on the cardiovascular disease have been reported. However, there is a paucity of studies on anti-atherosclerosis. Therefore, the anti-atherosclerosis potential of luteolin remains to be elucidated.MethodApoE-/- mice were fed with a high-fat diet to induce atherosclerosis in an animal model, where they were treated with oral administration of luteolin for 12 weeks. Primary mouse peritoneal macrophages challenged with oxidized low-density lipoprotein (oxLDL) were used for in vitro mechanistic study. The effectiveness of luteolin in the ApoE-/- mouse model of atherosclerosis was estimated in the aortic sinus and enface, and the underlying mechanisms were explored by molecular modeling study and siRNA-induced gene silencing.ResultsOur results showed that luteolin remarkably attenuated atherosclerosis in high-fat diet-induced ApoE-/- mouse via alleviating inflammation. We further found that luteolin decreased oxLDL-induced inflammation by inhibiting signal transducer and activator of transcription 3 (STAT3) in vitro, respectively. Further molecular modeling analysis indicated that luteolin interacted with STAT3 primarily through hydrogen bond interaction.ConclusionLuteolin could be a promising candidate molecule for atherosclerosis, and STAT3 may be a potential therapeutic target that could prevent the development of atherosclerosis.

Protective effect of luteolin on acute lung injury in sepsis mice

Objective To investigate the potential therapeutic effect of luteolin on sepsis-induced ALI and the underlying mechanisms. Methods Total of 50 mice were randomly(random number) divided into five groups: a sham control group, a sepsis-induced ALI group, and three sepsis groups pre-treated with 20, 40, and 80 mg/kg body weight luteolin. Mice in the treatment groups were pre-treated with luteolin at the respective oral dose two days before ALI induction. The lungs were isolated for histopathological examinations, and the bronchoalveolar lavage fluid (BALF) was collected for biochemical analyses. Results Luteolin significantly attenuated sepsis-induced ALI. Additionally, luteolin treatment decreased protein and inflammatory cytokine concentration and the number of infiltrated inflammatory cells in BALF compared with that in the non-treated sepsis mice. Pulmonary myeloperoxidase (MPO) activity was lower in the luteolin-pre-treated sepsis groups than in the sepsis group. The mechanism underlying the protective effect of luteolin on sepsis is related to the up-regulation of certain antioxidation genes, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), superoxide dismutases (SODs), and heme oxygenase 1 (HO-1), and the reduction of inflammatory responses through blockage of the activation of the nuclear factor (NF)-κB pathway. Conclusions Luteolin pre-treatment inhibits sepsis-induced ALI through its anti-inflammatory and antioxidative activity, suggesting that luteolin may be a potential therapeutic agent for sepsis-induced ALI. Key words: Luteolin; Sepsis; COX-2; SODs; iNOS

Protective effect of Luteolin against methyl methanesulfonate-induced toxicity

The third instar larvae of transgenic Drosophila were allowed to feed on the diet having 10 µM of MMS alone and along with 10, 20 and 40 µM of Luteolin for 24 hrs. After the completion of 24 hrs, the larvae were subjected to ONPG assay, X-gal staining, trypan blue exclusion test, oxidative stress markers, apoptosis and comet assays. A dose-dependent increase in GSH content and decrease in the β-galactosidase activity, tissue damage, GST activity, LPO, PCC, Caspase-9/3 activities, apoptotic index, and DNA damage was observed in the larvae exposed to 10, 20 and 40 µM of Luteolin along with 10 µM of MMS.

Protective effects of luteolin on rat testis following exposure to 900 MHz electromagnetic field

ABSTRACTIncreasing cell phone use calls for clarification of the consequences of long term exposure to electromagnetic fields (EMF). We investigated the effects of EMF on the testes of 12-week-old rats as well as possible protective effects of luteolin on testis tissue. Twenty-four Wistar albino rats were randomly divided into four groups: control, EMF, luteolin, and EMF + luteolin. The number of Leydig cells, primary spermatocytes and spermatids were reduced in the EMF group compared to the control group. In the EMF + luteolin group, the number of Leydig cells, primary spermatocytes and spermatids was significantly greater than the EMF group. We found an increase in superoxide dismutase (SOD) activity in the EMF group compared to the control group. In the EMF group, we found decreased wet weight of testes and serum testosterone levels compared to the control group. Decreased SOD enzyme activity, and increased serum testosterone levels and weight of the testes were observed in the EMF + luteolin group compared to the EMF group. EMF also affected sperm morphology. We found that in rat testis repeated exposure to 900 MHz EMF caused changes in testicular tissue and that the antioxidant, luteolin, substantially reduced the deleterious effects of EMF.

Protective effect of luteolin on the transgenic Drosophila model of Parkinson’s disease

In the present study we have studied the effect of 25, 50, 75 and 100 µM of luteolin on the transgenic Drosophila expressing human alpha synuclein. The doses of luteolin were established in diet and the PD flies were allowed to feed on it for 24 days. After 24 days of exposure the flies were assayed for climbing assay, oxidative stress markers, caspase-3 & 9 activity and dopamine content. The immunohistochemistry was also performed on the brain sections for the activity of tyrosine hydroxylase. The exposure of luteolin showed a dose dependent delay in the loss of climbing ability and activity, reduction in oxidative stress markers, caspase-3&9 activities and results in an increase in the dopamine content. The results obtained for the immunohistochemistry also supports the protective role of luteolin against the damage of the dopaminergic neurons.

Protective effect of luteolin on skin ischemia-reperfusion injury through an AKT-dependent mechanism.

Cutaneous ischemia-reperfusion (I/R) injury is one of the most crucial problems in flap surgery, which affects the survival of the skin flap and patient prognosis, luteolin, a plant derived flavonoid, has previously been shown to exert a variety of beneficial effects for reducing I/R injury in several organs. The aim of the present study was to evaluate the anti-inflammatory and anti-oxidative stress effects of luteolin on cutaneous I/R injury. The in vitro study were performed using a permanent human immortalized epidermal keratinocyte cell line (HaCaT), cells were cultured in the presence of luteolin and were then treated with hydrogen peroxide, the cell viability, mitochondrial membrane potential and the cell survival/apoptosis related signaling pathway activation were assessed to investigate the cytoprotective effects of luteolin. For in vivo experiments, skin flap I/R injury animal model was established in Sprague-Dawley rats, by measuring the area of flap survival, analyzing the expression of pro-inflammatory cytokine and evaluation of the histological changes in the skin tissue, the protective effects of luteolin on skin I/R injury were investigated. The function of protein kinase B (AKT) and heme oxygenase-1 (HO-1) activation on luteolin mediated I/R injury protection was assessed by administration of phosphoinositide-3-kinase/AKT inhibitor LY294002 and HO-1 inhibitor ZNPP. The results showed that luteolin treatment significantly increased the viability of HaCaT cells upon exposure to hydrogen peroxide, and the administration of luteolin in vivo significantly improved skin flap survival in the I/R injury rat model. The mechanisms underlying these beneficial effects included increased phosphoinositide-3-kinase/protein kinase B activation, improved expression of antioxidant enzyme, and scavenging the cytotoxic effects of reactive oxygen species (ROS). Taken together, the results suggested that luteolin preconditioning yielded significant protection against cutaneous I/R injury by protecting skin keratinocytes from ROS-induced damage.

Protective Effect of Luteolin Against Renal Ischemia/Reperfusion Injury via Modulation of Pro-Inflammatory Cytokines, Oxidative Stress and Apoptosis for Possible Benefit in Kidney Transplant.

BackgroundThe acceptances and long-term outcomes of the renal transplantations are seriously jeopardized by inflammatory responses and damage to tissues. The present study intended to explicate the pharmacological effect of luteolin (LT) in renal ischemia/reperfusion (I/R) injury and the possible mechanism of action of LT.Material/MethodsThe effect of LT on the level of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the homogenates of kidney tissues of male Swiss albino mice was determined after I/R injury. The effect of LT on MDA (malondialdehyde), SOD (superoxide dismutase), CAT (catalase), and glutathione were also identified by enzyme assay. In addition, Western blotting was used to determine the level of Bcl-2, Bax, and caspase-3 in the presence of LT.ResultsThe results showed that LT caused significant reduction in the level of TNF-α, IL-1β, and IL-6 compared to the I/R group without LT (p>0.05). To further confirm this, the efficacy of LT on the histopathology of I/R injured renal tissues was studied. It was found that LT restored cellular viability of damaged renal tissue. This observation was further confirmed by TUNEL assay, where it was found that LT caused considerable reduction in the population of apoptotic cells. LT pretreatment significantly increased Bcl-2 expression and reduced the level of Bax expression together with a reduction in the level of caspase-3 expression.ConclusionsLuteolin showed its effect by interfering and attenuating a number of pathways, including pathways for inflammation and apoptosis in renal tissues.

Protective Effects of Luteolin on Lipopolysaccharide-Induced Acute Renal Injury in Mice.

BackgroundSepsis can cause serious acute kidney injury in bacterium-infected patients, especially in intensive care patients. Luteolin, a bioactive flavonoid, has renal protection and anti-inflammatory effects. This study aimed to investigate the effect and underlying mechanism of luteolin in attenuating lipopolysaccharide (LPS)-induced renal injury.Material/MethodsICR mice were treated with LPS (25 mg/kg) with or without luteolin pre-treatment (40 mg/kg for three days). The renal function, histological changes, degree of oxidative stress, and tubular apoptosis in these mice were examined. The effects of luteolin on LPS-induced expression of renal tumor necrosis factor-α (TNF-α), NF-κB, MCP-1, ICAM-1, and cleaved caspase-3 were evaluated.ResultsLPS resulted in rapid renal damage of mice, increased level of blood urea nitrogen (BUN), and serum creatinine (Scr), tubular necrosis, and increased oxidative stress, whereas luteolin pre-treatment could attenuate this renal damage and improve the renal functions significantly. Treatment with LPS increased TNF-α, NF-κB, IL-1β, cleaved caspase-3, MCP-1, and ICAM-1 expression, while these disturbed expressions were reversed by luteolin pre-treatment.ConclusionsThese results indicate that luteolin ameliorates LPS-mediated nephrotoxicity via improving renal oxidant status, decreasing NF-κB activation and inflammatory and apoptosis factors, and then disturbing the expression of apoptosis-related proteins.