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Journal of Parenteral and Enteral Nutrition
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Original Communications

Sesame Oil Attenuates Hepatic Lipid Peroxidation by Inhibiting Nitric Oxide and Superoxide Anion Generation in Septic Rats

Dur-Zong Hsu, PhD1, Se-Ping Chien, MS4, Ya-Hui Li, MS1, Yin-Ching Chuang, MD5, Yu-Chung Chang, MD, PhD3 and Ming-Yie Liu, PhD1,2

From the 1 Department of Environmental and Occupational Health, 2 Sustainable Environment Research Centre, and 3 Department of Surgery, National Cheng Kung University Medical College, Tainan, Taiwan;4 Department of Living Science, Tainan University of Technology, Tainan, Taiwan; and 5 Department of Medicine, Chi-Mei Medical Center, Tainan, Taiwan.

Address correspondence to: Ming-Yie Liu, Department of Environmental and Occupational Health, National Cheng Kung University Medical College, 138 Sheng-Li Road, Tainan 704, Taiwan; e-mail: myliu{at}mail.ncku.edu.tw.

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.

Key Words: liver • lipid peroxidation • reactive oxygen species • nitric oxide • sepsis • sesame oil

Sepsis, a systemic inflammatory response syndrome, is one of the most common causes of mortality in intensive care units.1 Diverse molecular mechanisms of inflammation and cellular damage have been implicated in the pathogenesis of sepsis and multiple organ failure.2 Despite advances in critical care medicine, the mortality rate has not decreased significantly during the past 2 decades.3 In the United States, for example, > 200,000 patients die of sepsis every year.4 Lipid peroxidation results from the overgeneration of reactive oxygen species (ROS), which are known to be involved in the development of hepatic failure and death in sepsis.5 However, the effect of antioxidants used for managing sepsis is limited.6,7

ROS, including hydroxyl radical, superoxide anion, and nitric oxide (NO), are produced in animals and humans under pathophysiologic conditions8 such as sepsis.9,10 Hydroxyl radical, an extremely reactive species, is a crucial free radical involved in oxidative damage11 and produced primarily by the reaction of superoxide anion and NO.12-15 Superoxide anion is generated primarily from oxygen by activating xanthine oxidase,16 while NO is synthesized from L-arginine by the action of inducible NO synthase (iNOS) during sepsis-associated oxidative stress.17

Sesame oil, derived from the plant species Sesamum indicum L,18 has been used as a daily nutritional supplement to increase cell resistance to lipid peroxidation.19 Sesame oil increases the hepatic detoxification of chemicals and protects against oxidative stress.17,20 Our previous study showed that sesame oil decreased circulating hepatic enzymes and circulating oxygen free radicals in septic rats21; however, its effect on hepatic oxidative status has never been investigated. In the present study, we examined the effect of sesame oil on lipid peroxidation and oxygen free radical generation in liver in rats with cecal ligation and puncture (CLP)–induced sepsis.


   Methods
Top
Methods
Results
 Discussion
 
Materials
Sesame oil was obtained from Sigma (St Louis, MO).

Animals
Male SPF Wistar rats weighing 200-300 g were obtained from our institution's Laboratory Animal Center. They were individually housed in a room with a 12-hour dark/light cycle and central air conditioning (25°C, 70% humidity), allowed free access to tap water, and fed a rodent diet from Richmond Standard, PMI Feeds, Inc (St Louis, MO), with or without a sesame oil supplement. The animal care and experimental protocols were in accordance with nationally approved guidelines.

Experimental Design
We gave the rats oral sesame oil (4 mL/kg daily) or saline (4 mL/kg daily) for 1 week using a feeding cannula. We then induced sepsis using CLP and, 12 hours later, killed the rats using an intraperitoneal overdose of sodium pentothal (100 mg/kg).21 The rats were divided into 4 groups (8 rats in each group): 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. We did a hepatic histological examination 12 hours after inducing CLP and recorded lipid peroxidation, hydroxyl radical, superoxide anion, and nitrite levels in the liver tissue of all the rats. To further examine the sources of hepatic superoxide anion and NO, we determined xanthine oxidase and iNOS levels.

Surgical Procedures
The rats were anesthetized using light diethylether and then shaved over the anterior abdominal wall. A 2-cm-long midline incision, sufficient to expose the cecum and the adjacent intestine, was made. The ligated cecum was punctured twice with an 18-gauge needle, after which the cecum was gently squeezed to exude fecal matter. The abdominal incision was then closed, and 1 mL of saline was administered subcutaneously for fluid resuscitation.22,23

Blood Collection
Rat blood samples were collected from the femoral vein under light ethylether anesthesia 12 hours after a sham operation or CLP. Blood was drawn via venipuncture into serum separation tubes, allowed to clot for 30 minutes at room temperature, and then centrifuged at 1000g at 4°C for 10 minutes.

Measuring Lipid Peroxidation in the Liver
After we collected the blood samples, we killed the rats, excised their livers, and homogenized them in 20 mM Tris HCl (pH 7.4). The tissue homogenate (500 µL) was centrifuged at 2500g for 10 minutes at 4°C. The supernatant (200 µL) was analyzed for lipid peroxidation levels using a kit (Lipid Peroxidase Assay Kit; Merck Biosciences GmbH, Darmstadt, Germany), and the spectrophotometer (DU 640B; Beckman, Fullerton, CA) was read at 586 nm.22

Determining Hydroxyl Radical and Superoxide Anion in Liver
Briefly, the liver tissue was homogenized in Tris-sucrose buffer (0.24 M sucrose in 20 mM Tris HCl buffer containing 1 mM ethylenediaminetetra acetic acid [pH 7.4]) (1:10; w/v). The homogenate was centrifuged at 400g at 4°C for 30 minutes. Hydroxyl radical and superoxide anion were measured using a high-performance chemiluminescence (CL) analyzer (CLA-2100; Tohoku Electronic Industrial Co Ltd, Rifu, Japan). Whole-blood sample (400 µL) was mixed with 200 µL phosphate-buffered saline (PBS) in a stainless steel dish, and the background CL count was then read for 60 seconds. One hundred microliters of indoxyl β-D-glucuronide or lucigenin (17 mM dissolved in PBS, to determine hydroxyl radical and superoxide anion levels, respectively) was injected into the machine, and CL was counted for another 1200 seconds at 10-second intervals. The data were analyzed using Chemiluminescence Analyzer Data Acquisition Software (Tohoku Electronic Industrial Co).24,25

Measuring Nitrite Production in Liver Tissue
Briefly, we measured the nitrite levels in liver tissue following the Griess reaction. Liver tissue was homogenized in deionized water (1:10; w/v). Tissue homogenate (500 µL) was centrifuged at 2500g at 4°C for 10 minutes. Supernatant (100 µL) was incubated with 100 µL of Griess reagent at room temperature for 20 minutes. The absorbance was measured at 550 nm using a spectrophotometer. Nitrite concentration was calculated by comparing it with a standard solution of known sodium nitrite concentration.22,26

Determining iNOS in Liver Tissue
We homogenized liver tissue in ice-cold lysis buffer (1:10; w/v) containing 20 mM of Hepes (pH 7.2), 1% Triton X-100, 10% glycerol, 1 mM of PMSF, 10 µg/mL of leupeptin, and 10 µg/mL of aprotinin. We centrifuged this solution at 12,000 rpm for 30 minutes and then determined the protein concentration in the supernatant using protein assay dye (Bio-Rad Laboratories, Hercules, CA) with bovine serum albumin as the standard. We loaded 50 µg of protein on 8% or 10% sodium dodecyl sulfate polyacrylamide gel electrophoresis and then transferred it to nitrocellulose sheets (NEN Life Science Products, Inc, Boston, MA) in a transfer apparatus (Bio-Rad) run at 1.2 A for 3 hours. After we blocked the blots in 5% nonfat skim milk in TBST, we incubated the blots with primary iNOS polyclonal antibody (dilution 1:1000; BD Biosciences, Franklin Lakes, NJ) against target protein in 5% nonfat skim milk and then with antirabbit IgG conjugated with alkaline phosphatase (dilution 1:3000; Jackson ImmunoResearch Laboratories, Inc, Philadelphia, PA). Immunoblots were developed using BCIP/NBT solution (Kirkegaard & Perry Laboratories, Inc, Baltimore, MD).24,27 We relatively quantified the iNOS protein using densitometry with the ImageJ computer program (National Institutes of Health; available at http://rsb.info.nih.gov/ij/).

Determining Hepatic Xanthine Oxidase Activity
We assessed hepatic xanthine oxidase activity by measuring the uric acid concentration in serum. Serum levels of uric acid were evaluated using a blood biochemical analyzer (Fujifilm DRI-CHEM 3500 s; Fujifilm, Kanagawa, Japan).28

Statistical Analysis
Data are expressed as the means ± standard error of the mean (SEM). One-way ANOVA and then the Tukey honestly significant difference method were used to make pair-wise comparisons between the treatments in most experiments. Statistical significance was set at P < .05.


   Results
Top
Methods
 Results
Discussion
 
Sesame Oil Inhibited Hepatic Lipid Peroxidation in Septic Rats
Hepatic lipid peroxidation was significantly higher in the CLP group than in the sham, SO, and CS groups (P < .0001; Figure 1). This indicated that sesame oil potently and significantly (P < .0001) blocked oxidative stress by inhibiting hepatic lipid peroxidation in the CS group compared with the CLP group.


Figure 1
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  		Figure 1. Effects of sesame oil on hepatic lipid peroxidation (LPO) after cecal ligation and puncture (CLP) in rats. 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 a 1-week daily sesame oil supplement and then CLP. Hepatic LPO levels were determined 12 hours after CLP. Data are means ± SEM (n = 8). The differences between treatments with different letters are statistically significant (P < .05).

 

Sesame Oil Inhibited Hepatic ROS in Septic Rats
CLP-induced hepatic lipid peroxidation, hydroxyl radical, superoxide anion, and nitrite levels were significantly higher in the CLP group than in the other 3 groups (all Ps < .05; Figures 2, 3, 4). This showed that sesame oil significantly reduced ROS levels by inhibiting the generation of hydroxyl radical (Figure 2), superoxide anion (Figure 3), and nitrite (Figure 4).


Figure 2
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  		Figure 2. Effects of sesame oil on hepatic hydroxyl radical generation after cecal ligation and puncture (CLP) in rats. 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 a 1-week daily sesame oil supplement and then CLP. Hepatic hydroxyl radical (HR) count was determined 12 hours after CLP. Data are means ± SEM (n = 8). The differences between treatments with different letters are statistically significant (P < .05).

 

Figure 3
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  		Figure 3. Effects of sesame oil on hepatic superoxide anion productions after cecal ligation and puncture (CLP) in rats. 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 a 1-week daily sesame oil supplement and then CLP. Hepatic superoxide anion (SA) levels in the liver were determined 12 hours after CLP. Data are means ± SEM (n = 8). The differences between treatments with different letters are statistically significant (P < .05).

 

Figure 4
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  		Figure 4. Effects of sesame oil on hepatic nitrite production after cecal ligation and puncture (CLP) in rats. 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 a 1-week daily sesame oil supplement and then CLP. Hepatic nitrite levels were determined 12 hours after CLP. Data are means ± SEM (n = 8).

 
Sesame Oil Inhibited Xanthine Oxidase Activity but Not Xanthine Oxidase Protein Expression in Septic Rats
To investigate the inhibitory effect of sesame oil on the generation of superoxide anion, we assessed the activity and protein expression of xanthine oxidase. Neither CLP nor sesame oil affected hepatic xanthine oxidase expression in septic rats (data not shown). However, serum uric acid levels were significantly (P < .005) higher in the CLP group than in the sham and SO groups but significantly (P < .001) lower in the CS group than in the CLP group (Figure 5). This indicated that sesame oil significantly inhibited xanthine oxidase activity in septic rats.


Figure 5
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  		Figure 5. Effects of sesame oil on serum xanthine oxidase activity after cecal ligation and puncture (CLP) in rats. 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 a 1-week daily sesame oil supplement and then CLP. Serum uric acid levels were determined 12 hours after CLP. Data are means ± SEM (n = 8). The differences between treatments with different letters are statistically significant (P < .05).

 

Sesame Oil Inhibited Hepatic iNOS Expression in Septic Rats
To further confirm the inhibitory effect of sesame oil on NO production, we assessed hepatic iNOS expression. iNOS expression was significantly (P < .01) higher in the CLP group than in the other 3 groups (Figure 6), which showed that sesame oil inhibited iNOS expression and NO production in the CS group compared with the CLP group.


Figure 6
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  		Figure 6. Effects of sesame oil on hepatic inducible nitric oxide synthase (iNOS) expression after cecal ligation and puncture (CLP) in rats. 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 a 1-week daily sesame oil supplement and then CLP. Hepatic iNOS protein expression levels were determined 12 hours after CLP. Data are means ± SEM (n = 8). The differences between treatments with different letters are statistically significant (P < .05).

 

   Discussion
Top
Methods
 Results
 Discussion
 
Sesame oil might have attenuated hepatic lipid peroxidation by inhibiting hydroxyl radical, superoxide anion generations, and NO production in the livers of rats with CLP-induced sepsis. In addition, sesame oil inhibited xanthine oxidase activity and iNOS expression in sesame oil–associated reduction of superoxide anion and NO in septic rats.

Sesame oil also inhibited hepatic lipid peroxidation in rats with CLP-induced sepsis. Hepatic dysfunction is a major cause of death during sepsis; it is caused primarily by oxidative stress.22,25,29,30 Our previous study21 indicated that sesame oil potently decreased circulating oxygen free radicals and attenuated hepatic dysfunction in septic rats. In the present study, we showed that sesame oil inhibited hepatic lipid peroxidation and attenuated hepatic damage in septic rats. We hypothesize that the lower level of liver lipid peroxidation was important in sesame oil–associated hepatic protection during sepsis.

Sesame oil might have reduced hepatic lipid peroxidation by inhibiting ROS—hydroxyl radical, superoxide anion, and NO—the crucial mediators in the development of lipid peroxidation in CLP-induced sepsis.31 Hydroxyl radical reacts with membrane lipids, structural proteins and enzymes, or nucleotides, which leads to a profound alteration of cellular functions.32 In the present study, sesame oil potently decreased hepatic hydroxyl radical generation in septic rats. Therefore, we hypothesize that sesame oil might decrease lipid peroxidation by inhibiting hydroxyl radical generation in the liver. Furthermore, sesame oil significantly inhibited hepatic superoxide anion and NO production. Sesame oil might decrease hydroxyl radical–associated hepatic lipid peroxidation by suppressing superoxide anion and NO generation in rats with CLP-induced sepsis.

Inhibiting xanthine oxidase activity and iNOS expression might be involved in the anti-ROS effect of sesame oil in septic rats. Xanthine oxidase is a major source of superoxide anion in phagocytes, such as monocytes, macrophages, and neutrophils.16,33 On the other hand, iNOS expression in phagocytes is important in the overproduction of NO during sepsis.22,24 Sesame oil reduced xanthine oxidase activity and iNOS expression in CLP-induced septic rats. These observations are consistent with our previous study that sesame oil inhibits xanthine oxidase and iNOS in rats with lipopolysaccharide-induced sepsis.17,22,24 This indicates that sesame oil might decrease hepatic ROS by inhibiting the activation of xanthine oxidase and iNOS in rats with sepsis.

Furthermore, it is likely that sesame oil protected the liver by inhibiting the activation of hepatic phagocytes. After phagocytes are activated, they express iNOS, xanthine oxidase, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, all of which are associated with ROS generation34 and the development of oxidative stress.35-37 Although xanthine and NADPH oxidases (such as p22phox, p67phox, and p91phox) are involved in generating superoxide, xanthine oxidase is the major source of superoxide during sepsis.38-40 In the present study, sesame oil completely inhibited superoxide production and significantly decreased iNOS protein expression and xanthine oxidase activity. This indicated that sesame oil might affect the activation of hepatic phagocytes, such as Kupffer cells; however, more investigation of the effects of sesame oil on hepatic phagocytes will be needed. We conclude that sesame oil protects rats with CLP-induced sepsis from hepatic damage by at least partially inhibiting superoxide anion and NO generation, which in turn reduces hydroxyl radical–associated hepatic lipid peroxidation.


  
Top
Methods
 Results
 Discussion
 
Financial disclosure: This study was supported by grants NSC-96-2221-E-006-029-MY3, NSC-96-2314-B-006-012-MY2, and NSC-96-2628-B-006-038-MY3 from the National Science Council, Taiwan, and DOH92-TD-1009 from the Taiwan Department of Health.

Received for publication June 15, 2007. Accepted for publication October 5, 2007.

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Journal of Parenteral and Enteral Nutrition, Vol. 32, No. 2, 154-159 (2008)
DOI: 10.1177/0148607108314766
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