Protective Effect Of Luteolin Research Articles

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.

Protective effects of luteolin against acetaminophen-induced damage in L02 liver cells

This paper was aimed to investigate the protective effects of luteolin (Lut) against acetaminophen（APAP）-induced damage in L02 liver cells. CCK-8 was used to detect the cell activation of L02 cells treated by different Lut. The concentration and time of APAP induced L02 cell damage was screened. The effect of Lut on APAP induced apoptosis of L02 cells was detected by cell morphological observation, CCK-8 assay and flow cytometry. The contents of MDA, GSH and SOD activity in cell supernatant were detected by colorimetric assay. The expression of apoptosis-related genes Bax, Bcl-2 and caspase-3 was detected by RT-PCR. The results showed that Lut in 2.5-40 μmol•L⁻¹ range does not affect the activity of L02 cells; 12 mmol•L⁻¹ APAP incubated with L02 cell 12 h to establish damage model. Compared with the model group, the cell status of Lut group was significantly improved, the cell body was increased, the adherence ability was recovered, and the apoptosis rate was obviously decreased. MDA content decreased significantly (P<0.05, P<0.01), GSH and SOD activity significantly increased (P<0.05, P<0.01), at the same time, it could up-regulate expression of Bcl-2 mRNA and down-regulate the expression of Bax and caspase-3 mRNA. In conclusion,Lut has protective effect on APAP induced L02 cell injury, and its mechanism may be related to the reduction of oxidative stress and inhibition of apoptosis.

Protective effect of luteolin on streptozotocin-induced diabetic renal damage in mice via the regulation of RIP140/NF-кB pathway and insulin signalling pathway

Luteolin (LUT) is one of the most common flavonoids present in various fruits and vegetables. The effects of luteolin (LUT) on streptozotocin (STZ)-induced diabetic renal damage were investigated. LUT was orally administered at 10, 20 mg/kg/day for 4 weeks to streptozotocin-induced diabetic mice. Serum levels of uric acid, creatinine, triacylglycerol, total cholesterol, low density lipoprotein and blood urea nitrogen were measured. Urinary uric acid and creatinine were assayed. Serum insulin level and oral glucose tolerance test (OGTT) were determined. Kidney pathological changes were detected. Receptor-interacting protein 140 (RIP140)/nuclear factor кB (NF-кB) pathway and insulin signalling pathway were detected. LUT restored streptozotocin-induced insulin resistance, dyslipidaemia, hyperuricemia, and renal inflammatory cell infiltration in streptozotocin-induced mice. Furthermore, LUT inhibited RIP140/NF-кB pathway and improved the insulin signalling pathway in streptozotocin-induced renal damage in mice. Thus, the beneficial effect of LUT against diabetic nephropathy (DN) is related to its regulation of RIP140/NF-кB and insulin pathway.

Protective effects of luteolin against acetaminophen-induced acute liver failure in mouse.

Acetaminophen (APAP) is widely used as a safety analgesic and antipyretic agent. Although considered safe at therapeutic doses, overdose of APAP can cause acute liver injury that is sometimes fatal, requiring efficient pharmacological intervention. Luteolin is a naturally occurring flavonoid which is abundant in plants. The objective of this study was to investigate corresponding anti-oxidative and anti-inflammatory activities of luteolin, using acetaminophen-treated mice as a model system. Male C57BL/C mice were randomly divided into three groups (n=6 each). The control group was given phosphate buffered saline (PBS) orally. The APAP group was given APAP by intraperitoneal injection (i.p) at 300 mg/kg suspended in PBS. The luteolin-treated group was given APAP and luteolin (0-100 mg/kg/day, 1 or 3 days before APAP administration) suspended in PBS orally. 16 h after APAP administration, the liver and serum were collected to determine the liver injury. Luteolin administration significantly decreased acetaminophen-induced serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), malondialdehyde (MDA) levels, as well as glutathione (GSH) depletion and decrease of superoxide dismutase (SOD). Luteolin restored SOD, GSH and GSH-px activities and depressed the expression of pro-inflammatory factors, such as inducible nitric oxide synthase (i-NOS), TNF-α, nuclear factor kappa B (NF-κB), and IL-6, respectively. Moreover, luteolin down-regulated acetaminophen-induced nitrotyrosine (NT) formation and endoplasmic reticulum (ER) stress. These results suggest the presence of anti-oxidative, anti-inflammatory and anti-ER stress properties of luteolin in response to acetaminophen-induced liver injury in mice.

Luteolin attenuate the d-galactose-induced renal damage by attenuation of oxidative stress and inflammation

Luteolin is reported to have antioxidant and anti-inflammatory properties. In this study, we investigated the protective effect of luteolin against the renal damage induced by d-galactose (d-gal). The levels of creatinine (Cr) and urea nitrogen (BUN) were evaluated in plasma, kidney sections were stained with haematoxylin–eosin, followed by assessment of the antioxidant and anti-inflammatory activity. Furthermore, we also investigated the expression of the p38 mitogen-activated protein kinase (p38 MAPK) and its phosphorylated activation. The results of luteolin treatment showed that the renal damages were attenuated. Luteolin could significantly ameliorate d-gal-induced oxidative damage and suppress the inflammatory response. Moreover, the result also shows that luteolin could significantly inhibit the p38 MAPK phosphorylation in the kidneys from the model of d-gal-treated mice. Therefore, our research suggests that luteolin might be involved in the attenuated oxidative stress and inflammatory responses, hence the protective effects against d-gal-induced renal damage.