The protective effect of muscimol against systemic inflammatory response in endotoxemic mice is independent of GABAergic and cholinergic receptors.

Systemic inflammatory response syndrome plays an important role in the development of sepsis. GABAergic and cholinergic pathways activation are considered important for inflammatory response regulation. Tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-12, IL-10, as well as inducible nitric oxide synthase (iNOS)-derived nitric oxide (NO) are important inflammatory mediators involved in the pathogenesis of sepsis. Muscimol, an active compound from the mushroom Amanita muscaria (L.) Lam., is a potent GABAA agonist, inhibits inflammatory response via activating GABAA receptor and vagus nerve. However, the effect of muscimol on lipopolysaccharide (LPS)-induced systemic inflammatory response is still unclear. Therefore, we studied the effects of muscimol on systemic inflammatory response and survival rate in endotoxemic mice. Mice endotoxemia was induced by LPS. Muscimol was given to mice or RAW264.7 cells 30 min before LPS (10 mg/kg, i.p., or 10 ng/mL, respectively). Mice received GABAergic and cholinergic receptor antagonists 30 min before muscimol and LPS. Muscimol decreased TNF-α, IL-1ß, IL-12, iNOS-derived NO, and increased IL-10 levels and survival rate after LPS treatment. Muscimol significantly decreased nuclear factor kappa B (NF-κB) activity, increased IκB expression, and decreased pIKK expression in LPS-treated RAW264.7 cells. GABAergic and cholinergic antagonists failed to reverse muscimol's protection in LPS-treated mice. In conclusion, muscimol protected against systemic inflammatory response in endotoxemic mice may be partially independent of GABAergic and cholinergic receptors.

Ribosome Biogenesis Serves as a Therapeutic Target for Treating Endometriosis and the Associated Complications.

Ribosome biogenesis is a cellular process critical for protein homeostasis during cell growth and multiplication. Our previous study confirmed up-regulation of ribosome biogenesis during endometriosis progression and malignant transition, thus anti-ribosome biogenesis may be effective for treating endometriosis and the associated complications. A mouse model with human endometriosis features was established and treated with three different drugs that can block ribosome biogenesis, including inhibitors against mTOR/PI3K (GSK2126458) and RNA polymerase I (CX5461 and BMH21). The average lesion numbers and disease frequencies were significantly reduced in treated mice as compared to controls treated with vehicle. Flow cytometry analyses confirmed the reduction of small peritoneal macrophage and neutrophil populations with increased large versus small macrophage ratios, suggesting inflammation suppression by drug treatments. Lesions in treated mice also showed lower nerve fiber density which can support the finding of pain-relief by behavioral studies. Our study therefore suggested ribosome biogenesis as a potential therapeutic target for treating endometriosis.

Vestibular schwannomas: Accuracy of tumor volume estimated by ice cream cone formula using thin-sliced MR images.

PURPOSE: We estimated the volume of vestibular schwannomas by an ice cream cone formula using thin-sliced magnetic resonance images (MRI) and compared the estimation accuracy among different estimating formulas and between different models. METHODS: The study was approved by a local institutional review board. A total of 100 patients with vestibular schwannomas examined by MRI between January 2011 and November 2015 were enrolled retrospectively. Informed consent was waived. Volumes of vestibular schwannomas were estimated by cuboidal, ellipsoidal, and spherical formulas based on a one-component model, and cuboidal, ellipsoidal, Linskey's, and ice cream cone formulas based on a two-component model. The estimated volumes were compared to the volumes measured by planimetry. Intraobserver reproducibility and interobserver agreement was tested. Estimation error, including absolute percentage error (APE) and percentage error (PE), was calculated. Statistical analysis included intraclass correlation coefficient (ICC), linear regression analysis, one-way analysis of variance, and paired t-tests with P < 0.05 considered statistically significant. RESULTS: Overall tumor size was 4.80 ± 6.8 mL (mean ±standard deviation). All ICCs were no less than 0.992, suggestive of high intraobserver reproducibility and high interobserver agreement. Cuboidal formulas significantly overestimated the tumor volume by a factor of 1.9 to 2.4 (P ≤ 0.001). The one-component ellipsoidal and spherical formulas overestimated the tumor volume with an APE of 20.3% and 29.2%, respectively. The two-component ice cream cone method, and ellipsoidal and Linskey's formulas significantly reduced the APE to 11.0%, 10.1%, and 12.5%, respectively (all P < 0.001). CONCLUSION: The ice cream cone method and other two-component formulas including the ellipsoidal and Linskey's formulas allow for estimation of vestibular schwannoma volume more accurately than all one-component formulas.

[Recurrence of Cerebral Infarction Associated Aspirin Resistance or Chinese Medical Constitutions: a Correlation Study].

OBJECTIVE: To explore the correlation between the recurrence of cerebral infarction and aspirin resistance (AR)/Chinese medical (CM) constitutions. METHODS: Totally 413 cerebral infarction patients took Aspirin Enteric-coated Tablet (100 mg per day) while receiving routine therapy, 5 days at least in a week. They were followed-up for 12 months. Aspirin sensitivity (AS) was determined using turbidimetry. CM constitutions among patients with different AS were compared. Ratios of AR patients and AS patients of different CM constitutions in cerebral infarction recurrent patients were compared. Platelet membrane glycoproteins (GP) II b HPA-3 gene polymorphism was detected by polymerase chain reaction (PCR) method. Correlation between recurrence of cerebral infarction and AR, bb genotypes, CM constitutions times AS were analyzed by Logistic regression. RESULTS: Totally 11 patients dropped out, 101 (25.12%)with recurrent cerebral infarction and 301 (74.88%) without recurrent cerebral infarction. There were 152 (37.81%) AR patients and 250 (62.19%) AS patients. AR accounted for 26.6% (80/ 301) and AS accounted for 73.4% (221/301) in non-recurrent cerebral infarction patients. AR accounted for 71.3% (72/101) and AS accounted for 28.7% (29/101) in recurrent cerebral infarction patients. There was statistical difference in AR and AS ratios (χ2 = 64.287, P = 0.000). The proportion of yin deficiency constitution (YDC) was the largest [28.3% (43/152)] in AR patients. The proportion of blood stasis constitution (BSC) was the largest [23.6% (59/250)] in AS patients. There was statistical difference in CM constitutions between AR patients and AS patients (χ2 = 21.574, P < 0.01). The former 4 recurrent rates occurred in AR patients of YDC, BSC, damp-phlegm constitution (DPC), qi deficiency constitution (QDC). YDC occupied the first place [22.4% (34/152)]. The former 4 recurrent rates occurred in AS patients of BSC, QDC, DPC, damp-heat constitution (DHC). BSC occupied the first place [3.2% (2/250)]. Compared with non-recurrent cerebral infarction patients and AS patients, bb gene occurred most often, but aa gene and ab gene occurred obviously lesser in non-recurrent cerebral infarction patients and AR patients (χ2 = 20.171, χ2 = 55.139, P < 0.01). AR and bb gene were positively correlated with recurrent cerebral infarction (OR = 18.423, P = 0.000; OR = 1.304, P = 0.028). Body constitutions interacted with AS (OR = 0.707, P = 0.000). CONCLUSIONS: Recurrent cerebral infarction was closely related to AR and constitutional types. The recurrence rate was higher in AR patients of YDC. GP I b HPA-3 bb genotype might be a risk factor for AR and recurrent cerebral infarction.

Sesamol ameliorates hypotension by modulating cytokines and PPAR-gamma in systemic inflammatory response.

Sepsis is one of the major causes of death reported in intensive care units. Acute kidney injury (AKI) and hypotension are important in the pathogenesis and mortality of systemic inflammatory response (SIR). Sesamol delays mortality in sepsis; however, its effects on AKI and hypotension and the role of peroxisome proliferator-activated receptor-É£ (PPAR-γ) activation have not been established. We investigated the effect of sesamol on SIR in cecal ligation and puncture (CLP)-induced acute kidney injury and lipopolysaccharide (LPS)-induced hypotension in rats. Sesamol was subcutaneously injected 1 h after SIR. Renal function (BUN and CRE) and proinflammatory mediators interleukin (IL)-1ß and IL-6 were increased after CLP. Tumor necrosis factor (TNF)-α, IL-1ß, IL-10, and nitrite production were significantly increased 6 h after LPS-induced hypotension (mean arterial pressure was significantly decreased). Sesamol significantly inhibited BUN, CRE, IL-1ß, IL-6, and nitrite after CLP-induced acute renal injury. In addition, sesamol increased mean arterial pressure and IL-10, inhibited TNF-α and IL-1ß, but did not affect nitrite production in LPS-induced hypotension. Sesamol increased PPAR-γ in the leucocytes and peritoneal macrophages in LPS-induced SIR. We conclude that sesamol regulates leucocyte and macrophage PPAR-γ-associated systemic cytokines expression, thereby ameliorates acute kidney injury and hypotension in rats.

Sesame oil attenuates ovalbumin-induced pulmonary edema and bronchial neutrophilic inflammation in mice.

BACKGROUND: Allergic asthma is one of the most common chronic inflammatory diseases of airways. Severe asthma may lead to hospitalization and death. Sesame oil is a natural product with anti-inflammatory property. However, the effect of sesame oil on allergic asthma has never been studied. OBJECTIVE: We investigate the effect of sesame oil on pulmonary inflammation in allergic asthma model. METHODS: Allergic airway inflammation was induced by sensitizing with two doses of 10 mg ovalbumin (OVA) and then challenged with 1% OVA nebulizer exposure (1 h/day) for 3 days. Sesame oil (0.25, 0.5, or 1 mL/kg/day) was given orally 30 min before each challenge. Samples were collected 24 h after the last challenge. RESULTS: Data showed that sesame oil inhibited pulmonary edema and decreased interleukin (IL)-1 ß and IL-6 levels in bronchoalveolar lavage fluid in OVA-treated mice. Sesame oil also decreased pulmonary nitrite level, inducible nitric oxide synthase expression, and neutrophil infiltration induced by OVA. Further, sesame oil decreased serum IgE level in OVA-treated mice. CONCLUSION: Sesame oil may attenuate pulmonary edema and bronchial neutrophilic inflammation by inhibiting systemic IgE level in allergic asthma.

Role of flavin-containing-monooxygenase-dependent neutrophil activation in thioacetamide-induced hepatic inflammation in rats.

Thioacetamide is widely used in industry and is known to be one of the most potent hepatotoxicants in experimental animals. We investigated the involvement of flavin-containing monooxygenase (FMO)-dependent hepatic-neutrophil activation and the release of proinflammatory mediators in thioacetamide-induced hepatic injury in rats. Thioacetamide (100 mg/kg, intraperitoneally) increased, within 12 h, hepatic serum aspartate transferase and alanine transferase levels, tumor necrosis factor-α production, interleukin-1ß and nitrite levels, and myeloperoxidase activity. Rabbit anti-neutrophil serum markedly inhibited all thioacetamide-altered parameters. In addition, FMO-competitive inhibitor methimazole reduced thioacetamide-induced myeloperoxidase activity, hepatic tumor necrosis factor-α, interleukin-1ß, nitrite, inducible nitric oxide synthase, and hepatic damage in thioacetamide-treated rats. Thus, we conclude that FMO-dependent hepatic neutrophil activation initiates the release of proinflammatory mediators in thioacetamide-treated rats.

Prophylactic and therapeutic effects of a subcutaneous injection of sesame oil against iron-induced acute renal injury in mice.

BACKGROUND: Iron intoxication causes acute nephrotoxicity in animals and humans. Sesame oil, a healthful food, increases resistance to lipid peroxidation and protects against multiple organ injury in various animal models. The authors examined the prophylactic and therapeutic effects of a subcutaneous injection of sesame oil against iron-induced acute renal injury in mice. METHODS: Iron intoxication in mice was induced with an intraperitoneal injection (2 mg/kg) of ferric-nitrilotriacetate (Fe-NTA). Various doses of sesame oil (0, 1, 2, and 4 mL/kg, subcutaneously) were given immediately after (prophylactic) or 30 minutes after (therapeutic) the Fe-NTA injection. Renal injury was assessed by the rise in serum blood urea nitrogen (BUN) and creatinine (CRE) levels 3 hours after the Fe-NTA injection. RESULTS: One hour after the Fe-NTA injection, serum BUN and CRE levels were significantly higher in Fe-NTA-treated mice than in saline-treated controls; 3 and 6 hours after the Fe-NTA injection, they were dose-dependently and significantly lower in all sesame oil-treated groups than in the group treated only with Fe-NTA and saline. CONCLUSION: A subcutaneous injection of sesame oil had both prophylactic and therapeutic effects against iron-induced acute renal injury in mice.

Sesame oil prevents acute kidney injury induced by the synergistic action of aminoglycoside and iodinated contrast in rats.

The aim of the study was to investigate the effect of sesame oil on acute kidney injury induced by the synergistic action of aminoglycoside and iodinated contrast in rats. Acute kidney injury was induced by a 5-day course of daily gentamicin injections (100 mg/kg of body weight, subcutaneously) and then iodinated contrast (4 ml/kg, intravenously) in male specific-pathogen-free Sprague-Dawley rats. Sesame oil (0.5 ml/kg, orally) was given 1 h before iodinated contrast. Renal function and oxidative stress were assessed 6 h after iodinated contrast injection. Renal function was evaluated by measuring serum blood urea nitrogen and creatinine levels. Renal oxidative stress was assessed by determining renal lipid peroxidation, myeloperoxidase, hydroxyl radical, superoxide anion, nitrite/nitrate, and inducible nitric oxide synthase levels. Sesame oil significantly prevented the rise of serum blood urea nitrogen and creatinine levels. Furthermore, there was a parallel inhibition of the rise in levels of expression of renal lipid peroxidation, myeloperoxidase, hydroxyl radicals, superoxide anion, nitrite/nitrate, and inducible nitric oxide synthase in rats with gentamicin-plus-iodinated contrast-induced acute kidney injury. We conclude that sesame oil may attenuate aminoglycoside-plus-iodinated contrast-induced acute kidney injury by inhibiting renal oxidative stress in rats.

Ostensibly ineffectual doses of cadmium and lipopolysaccharide causes liver damage in rats.

Various hepatotoxicants co-treated with lipopolysaccharide (LPS) have the potential to cause severe hepatic damage. Whether co-treatment with ostensibly ineffectual (without effect on customary clinical liver function tests, such as aspartate aminotransferase and alanine aminotransferase) doses of cadmium (Cd) and LPS cause liver damage is still unknown. We examined the effects of treating ostensibly ineffectual doses of Cd and LPS on liver dysfunction as well as on liver histopathology. We injected rats with saline only, Cd only, LPS only, or a single ostensibly ineffectual dose of Cd (100 µg/kg body weight) plus LPS (0.1 mg/kg body weight). After 6 h, the rats were killed and their liver damage was assessed. Co-treated with ostensibly ineffectual doses of Cd and LPS had higher levels of aspartate aminotransferase and alanine aminotransferase, hepatic lipid peroxidation, peroxynitrite, nitrite, and interleukin-1ß (IL-1ß), but lower levels of hepatic metallothionein (MT) than did that treated with saline only, Cd only, and LPS only. Histopathological analysis of Cd only and LPS only showed apparent liver damage, but Cd plus LPS showed marked hepatic damage. We conclude that co-treating the rats with ostensibly ineffectual doses of Cd and LPS is hepatotoxic. Cd promotes LPS-initiated oxidative-stress-associated liver damage by increasing IL-1ß and decreasing MT levels in rats.

[Short hairpin RNA targeting N-acetylglucosaminyltransferase V inhibits the proliferation of prostate cancer PC-3 cell line].

OBJECTIVE: To investigate the effect of short hairpin RNA (shRNA) targeting N-acetylglucosaminyltransferase V (GnT-V) on the proliferation of prostate cancer PC-3 cells. METHODS: Lipofectamine 2000 was used to transfect the recombinant plasmids carrying the shRNA targeting GnT-V gene into PC-3 cells. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to measure the mRNA expression of GnT-V, and CCK-8 assay was used to measure the cell proliferation after the transfection. RESULTS: The recombinant plasmids were successfully transfected into PC-3 cells, resulting in a reduction of GnT-V mRNA expression by 73%. The proliferation of PC-3 cells was significantly inhibited after the transfection. CONCLUSION: The shRNA targeting GnT-V gene can reduce the expression of GnT-V mRNA and inhibit the proliferation of PC-3 cells in vitro.

Protective effect of daily sesame oil supplement on gentamicin-induced renal injury in rats.

Gentamicin, an aminoglycoside antibiotic, is widely used in the treatment of Gram-negative infections; however, dose-limiting nephrotoxicity restricts its optimal use. We investigated the effect of a daily sesame oil supplement on oxidative-stress-associated renal injury induced by a single daily dose of gentamicin in rats. Renal injury was induced by a single subcutaneous daily dose of gentamicin (100 mg kg(-1) d(-1) for 7 days), and then the effects of oral sesame oil (0.25, 0.5, and 1 mL kg(-1) d(-1) for 7 days) on renal injury, oxidative stress, hydroxyl radical, superoxide anion, and NO were assessed after treatment. Sesame oil inhibited gentamicin-induced renal injury, lipid peroxidation, hydroxyl radical, and superoxide anion, as well as NO production. In addition, sesame oil inhibited xanthine oxidase activity and inducible NOS expression in gentamicin-challenged rats. We hypothesize that a daily sesame oil supplement attenuates oxidative-stress-associated renal injury by reducing oxygen free radicals and lipid peroxidation in gentamicin-treated rats.

Sesame oil attenuates hepatic lipid peroxidation by inhibiting nitric oxide and superoxide anion generation in septic rats.

BACKGROUND: Sepsis is a major cause of mortality in the intensive care unit. Oxidative stress plays an important role in the pathogenesis of organ failure during sepsis. Sesame oil decreases circulating oxygen free radicals in septic rats; however, its effect on hepatic oxidative status is unknown. The authors examined the effect of sesame oil on hepatic lipid peroxidation in septic rats. METHODS: Hepatic injury was induced using cecal ligation and puncture (CLP). Rats were divided into 4 groups: sham, rats given a sham operation without CLP; SO, rats given sesame oil alone; CLP, rats given saline and then CLP; and CS, rats given sesame oil and then CLP. All rats were first given a 1-week daily oral supplement of sesame oil or saline (4 mL/kg/d) and then CLP or a sham operation. The authors assessed hepatic oxidative stress by determining hepatic lipid peroxidation, hydroxyl radical, superoxide anion, and nitric oxide levels 12 hours after CLP. They also assessed xanthine oxidase activity and nitric oxide synthase expression. RESULTS: Hepatic lipid peroxidation (P < .0001), hydroxyl radical (P < .05), superoxide anion (P < .05), and nitrite (P < .05) levels were significantly lower in sesame oil-treated septic rats. Furthermore, sesame oil significantly reduced xanthine oxidase activity (P < .01) and inducible nitric oxide synthase expression (P < .005) in septic rats. CONCLUSIONS: Sesame oil might attenuate hepatic lipid peroxidation by inhibiting superoxide anion and nitric oxide, at least partially, in experimental septic rats.

Sesame oil does not show accumulatively enhanced protection against oxidative stress-associated hepatic injury in septic rats.

BACKGROUND: Sepsis is one of the major causes of death reported in intensive care units. A daily supplement of sesame oil for 1 week significantly attenuates oxidative stress-associated hepatic injury in septic rats. However, the excess intake of sesame oil may be associated with a health risk. This study investigates the effect of accumulative sesame oil on oxidative stress-associated hepatic injury after cecal ligation and puncture in rats. METHODS: Sesame oil was administered daily (4 mL/kg/d, orally) to rats, and the total intake of sesame oil ranged from 0 (control) to 140 mL/kg before cecal ligation and puncture in 9 groups of rats. Oxidative stress was examined by determining the levels of lipid peroxidation and glutathione. Hepatic injury was evaluated by measuring serum levels of aspartate aminotransferase and alkaline phosphatase. RESULTS: Rats that received sesame oil for 4 and 5 weeks had a lower body weight gain compared with those that received saline. Lipid peroxidation was decreased in the 20-mL/kg and 28-mL/kg groups, but it was increased in the 140-mL/kg group compared with the control group. Glutathione levels were increased in the < or =28-mL/kg groups compared with the control group. Serum levels of aspartate aminotransferase and alkaline phosphatase were reduced in the < or =28-mL/kg groups compared with the control group. CONCLUSION: Sesame oil does not demonstrate accumulatively enhanced protection against oxidative stress-associated hepatic injury after cecal ligation and puncture in rats.

Sesame oil protects against lead-plus-lipopolysaccharide-induced acute hepatic injury.

Lead (Pb) increases lipopolysaccharide (LPS)-induced tumor necrosis factor alpha, which causes liver damage. In this study, we investigated the effect of sesame oil on Pb-plus-LPS (Pb + LPS)-induced acute liver damage in mice. Mice were given sesame oil (8 mL/kg orally) just after Pb acetate (10 mmol/kg i.p.) plus LPS (5 mg/kg i.p.). Aspartate aminotransferase, alanine aminotransferase, tumor necrosis factor-alpha, interleukin-1beta, nitric oxide, and inducible nitric oxide synthase levels were examined. Sesame oil significantly decreased serum aspartate aminotransferase and alanine aminotransferase levels in Pb + LPS-stimulated mice. Sesame oil reduced Pb + LPS-induced tumor necrosis factor-alpha, interleukin-1beta, and nitric oxide production in serum and liver tissue. Furthermore, sesame oil decreased inducible nitric oxide synthase expression in leukocytes and liver tissue in Pb + LPS-treated mice. We hypothesize that the inhibition of proinflammatory cytokines and nitric oxide might be involved in sesame oil-associated protection against Pb + LPS-induced acute hepatic injury in mice.

Sesame oil attenuates Cisplatin-induced hepatic and renal injuries by inhibiting nitric oxide-associated lipid peroxidation in mice.

Although cisplatin (cis-diamminedichloroplatinum) is an effective drug for the treatment of several solid tumors and has been used therapeutically for decades, several cisplatin-induced side effects have limited its therapeutic dosage in clinical studies. Our aim was to examine the effect of sesame oil on cisplatin-induced hepatic and renal injuries in mice (8-week-old female SPF C57BL/6) given subcutaneous cisplatin (0, 5, 10, or 20 mg/kg). Hepatic and renal functions, lipid peroxidation (LPO) levels, and reactive oxygen free radicals were evaluated 3 days after cisplatin administration, and tumor volumes were recorded 0, 3, 6, and 9 days after cisplatin administration. Sesame oil (i) potently attenuated cisplatin-associated hepatic and renal injuries; (ii) decreased cisplatin-initiated LPO as well as the production of hydroxyl radical, peroxynitrite, and nitrite in blood and tissue; and (iii) did not affect the antitumor capacity exerted by cisplatin in mice with melanoma. We suggest that sesame oil attenuates cisplatin-induced hepatic and renal damage by at least partially inhibiting nitric oxide-associated LPO in mice. Sesame oil might be a new approach for preventing cisplatin-induced multiple organ injury during the treatment of tumors.

Sesame oil attenuates acute iron-induced lipid peroxidation-associated hepatic damage in mice.

Acute iron intoxication from the accidental ingestion of iron-containing preparations is one important cause of death in children. The aim of this study was to investigate the protective effect of sesame oil on acute iron-induced lipid peroxidation (LPO) and hepatic injury in mice. Acute iron intoxication was induced by giving ferric nitrilotriacetate to mice. Hepatic function was assessed using blood biochemistry. Free radicals were determined using a high-performance chemiluminescence analyzer. Ferric nitrilotriacetate increased serum ferrous (Fe) and LPO levels, and induced acute hepatic injury. Sesame oil (a) dose-dependently decreased acute iron-induced LPO and hepatic injury, (b) reduced acute iron-associated hydroxyl radical and superoxide anion generation, and (c) inhibited the activity of xanthine oxidase in acute iron intoxication. Thus, sesame oil might ameliorate LPO and acute hepatic injury by inhibiting xanthine oxidase-initiated superoxide anion generation, thereby reducing hydroxyl radical production, at least partially, in acutely iron-intoxicated mice.

Effect of sesame oil on oxidative-stress-associated renal injury in endotoxemic rats: involvement of nitric oxide and proinflammatory cytokines.

This study aimed to investigate the effect of sesame oil on oxidative stress-associated renal injury induced by lipopolysaccharide in rats. The effects of sesame oil on renal injury, oxidative stress, hydroxyl radical, superoxide anion, nitric oxide, and proinflammatory cytokines were assessed after a lipopolysaccharide challenge. Sesame oil attenuated lipopolysaccharide-induced renal injury, decreased lipid peroxidation, increased the activities of superoxide dismutase, catalase, and glutathione peroxidase, reduced hydroxyl radical generation and nitric oxide production, and had no effect on superoxide anion generation in lipopolysaccharide-challenged rats. In addition, sesame oil significantly decreased tumor necrosis factor-alpha and interleukin 1beta production 1 and 6 h, respectively, after lipopolysaccharide administration in mice. Thus, sesame oil attenuates oxidative stress-associated renal injury via reduction of the production of nitric oxide and the generation of proinflammatory cytokines in endotoxemic rats.

Effects of sesame oil on oxidative stress and hepatic injury after cecal ligation and puncture in rats.

Oxidative stress is known to be involved in the development of organ failure and death in sepsis. Sesame oil attenuates oxidative stress induced by endotoxin; however, whether sesame oil is still effective in rats with sepsis has never been investigated. The aim of the present study was to determine the effect of sesame oil on oxidative stress-associated hepatic injury in cecal ligation and puncture-induced rats with sepsis. We examined the effect of sesame oil (4 mL/kg daily for 1 week) on lipid peroxidation, hydroxyl radical, superoxide anion, and nitrite levels in rats with sepsis. In addition, hepatic injury was also assessed by blood biochemistry. Sesame oil significantly decreased lipid peroxidation and serum nitrite levels, but affected neither superoxide anion nor hydroxyl radical in cecal ligation and puncture-treated rats. Furthermore, sesame oil significantly attenuated cecal ligation and puncture-induced hepatic injury in rats. Nevertheless, oxidative stress and hepatic injury were not affected by corn oil or mineral oil in rats with sepsis. Thus, attenuation of oxidative stress and hepatic injury may be associated with inhibition of nitric oxide in sesame oil-associated protection in rats with sepsis.