scholarly journals Protective Effect of Thymus serrulatus Essential Oil on Cadmium-Induced Nephrotoxicity in Rats, through Suppression of Oxidative Stress and Downregulation of NF-κB, iNOS, and Smad2 mRNA Expression

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1252
Author(s):  
Mohd Nazam Ansari ◽  
Najeeb Ur Rehman ◽  
Aman Karim ◽  
Faisal Imam ◽  
Abubaker M. Hamad
Keyword(s):  
Oxidative Stress ◽  
Essential Oil ◽  
Protective Effect ◽  
Mrna Expression ◽  
Kidney Function ◽  
Normal Control ◽  
Control Group ◽  
Standard Group ◽  
Enzymatic Antioxidants ◽  
Experimental Protocol

The purpose of the research was to examine the protective effect of essential oil from Thymus serrulatus Hochst. ex Benth. (TSA oil) against cadmium (Cd)-induced renal toxicity. The experimental protocol was designed using 30 healthy adult Wistar albino rats allocated into five groups containing six animals in each group. Group 1 was treated as normal control and groups 2, 3, 4, and 5 were treated with cadmium chloride (CdCl2, 3 mg/kg, IP) for 7 days. Group 3 was also treated with silymarin (100 mg/kg, PO) as a standard group, while groups 4 and 5 were administered with TSA oil at doses of 100 and 200 mg/kg PO, respectively. The nephrotoxicity was measured with various parameters such as kidney function markers, oxidative stress markers (glutathione (GSH) and malondialdehyde (MDA)), and messenger ribonucleic acid (mRNA) expression levels of inflammatory factors. The histological studies were also evaluated in the experimental protocol. The CdCl2-treated groups showed a significant increase in the levels of serum kidney function markers along with MDA levels in kidney homogenate. However, renal GSH level was found to be reduced significantly. It was found that CdCl2 significantly upregulated the nuclear factor levels of kappaB (NF-κB p65), inducible nitric oxide synthase (iNOS), and small mothers against decapentaplegic (Smad2) as compared to the normal control group. On the other hand, TSA oil significantly improved the increased levels of serum kidney function markers, non-enzymatic antioxidants, and lipid peroxidation. In addition, TSA oil significantly downregulated the increased expression of NF-κB p65, iNOS, and Smad2 in Cd-intoxicated rats. Moreover, the histological changes in the tissue samples of the kidney of Cd-treated groups were significantly ameliorated in the silymarin- and TSA-oil-treated groups. The present study reveals that TSA oil ameliorates Cd-induced renal injury, and it is also proposed that the observed nephroprotective effect could be due to the antioxidant potential of TSA oil and healing due to its anti-inflammatory action.

scholarly journals Neurological Alterations and Testicular Damages in Aging Induced by D-Galactose and Neuro and Testicular Protective Effects of Combinations of Chitosan Nanoparticles, Resveratrol and Quercetin in Male Mice

Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 435
Author(s):  
Reham Z. Hamza ◽  
Mohammad S. Al-Harbi ◽  
Munirah A. Al-Hazaa
Keyword(s):  
Oxidative Stress ◽  
Chitosan Nanoparticles ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Wide Range ◽  
Neurological Alterations

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.

Protective effect of GSK-3β/Nrf2 mediated by dimethyl fumarate in middle cerebral artery embolization reperfusion rat model

2021 ◽  
Vol 18 ◽  
Author(s):  
Yuan Li ◽  
Lan Chu ◽  
Chunfeng Liu ◽  
Zongyi Zha ◽  
Yuanlu Shu
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Sham Group ◽  
Infarct Volume ◽  
Dimethyl Fumarate ◽  
Control Group ◽  
Related Factor ◽  
Nissl Staining ◽  
Gsk 3Β ◽  
Nrf2 Expression

Aim: This study investigated the protective effect of dimethyl fumarate (DMF) in rats by mediating GSK3-β/Nrf2 using the middle cerebral artery embolization reperfusion (MCAO/R) rat model. Background: After an acute ischemic stroke (AIS), oxidative stress occurs. Dimethyl fumarate (DMF), a nuclear factor-E2-related factor 2 (Nrf2) activator, approved by the US Food and Drug Administration (FDA), was observed to regulate the Nrf2 pathway by acting as an anti-oxidative stress agent; however, whether this agent is involved in inhibiting GSK-3β remains to be established. Methods: DMF model was used to explore the effects of GSK-3β on Nrf2 expression level, Nrf2-ARE binding activity and Nrf2/ARE downstream expression level of anti-oxidant stress protein in Cerebral ischemia-reperfusion injury (CIRI). 60 rats were randomly divided into Sham group, MCAO/R group, solvent control group (DMSO group) and DMF treatment group, with 15 rats in each group. The MCAO/R, DMSO and DMF groups were considered in the MCAO/R model using the modified thread embolization method. In contrast, the Sham group was only anaesthetized and disinfected, and tissue muscle was dissected without inserting suture emboli. DMF group was gavaged with 45mg/kg per day of DMF, DMSO control group was gavaged with DMSO of equal volume, while MCAO/R group was only modeled without any intragastric treatment. The rats were treated seven days after the operation, and a neurological function Longa score was estimated. The rats were sacrificed seven days later, and the infarct volume was assessed by TTC staining. Hematoxylin-eosin (HE) staining was used to observe the pathological changes in rat brain tissue. Nissl staining was used to observe the expression of neurons in the infarcted cortex. Western blotting (WB) was used to observe the protein expression levels of glycogen synthase kinase 3β(GSK-3β), nuclear factor E2-related factor 2 (Nrf2), downstream heme oxygenase 1 (HO1) and NADPH quinone oxidoreductase 1 (NQO1) in four groups. The expression levels of GSK-3β and Nrf2 in the four groups were observed by immunohistochemistry and immunofluorescence. Results: (1) The Longa score of the MCAO/R, DMSO and DMF groups was found to be higher compared to the Sham group, indicating successful operation. The Longa score of the DMF group was lower than that of the other three groups 4-7 days after surgery (P<0.05). (2) HE and Nissl staining showed that the DMF group had lower neuron necrosis and higher gliosis compared to the control groups. (3) TTC staining results showed that the infarct volume of the DMF group was significantly smaller than the MCAO/R and DMSO groups. (4) Protein results showed that the GSK-3β expression in the DMF group was lower than that in all groups, while the expression of Nrf2, HO1 and NQO1 was higher compared to other groups. Conclusion: DMF can reduce neurological deficits and infarct size in the MCAO/R model. The protective effect may be related to decreased GSK-3β expression and increased Nrf2 expression, which may play a role in anti-oxidative stress.

Protective effect of essential oil from Citrus limon against aspirin-induced toxicity in rats

2018 ◽  
Vol 38 (5) ◽  
pp. 499-509 ◽  
Author(s):  
H Bouzenna ◽  
N Samout ◽  
S Dhibi ◽  
S Mbarki ◽  
S Akermi ◽  
...  
Keyword(s):  
Essential Oil ◽  
Protective Effect ◽  
Antioxidant Activities ◽  
Reducing Power ◽  
Female Rats ◽  
Control Group ◽  
Albino Rats ◽  
Citrus Limon ◽  
Β Carotene ◽  
Aspirin Group

The present study is planned to examine the antioxidant activity (AA) and the protective effect of the essential oil of Citrus limon (EOC) against aspirin-induced histopathological changes in the brain, lung, and intestine of female rats. For this purpose, 28 albino rats were classified to control group (group C), aspirin group (group A), EOC group (group EOC), and pretreatment with EOC and treated with aspirin group (group EOC + A). The antioxidant activities of EOC were evaluated by three different assays including reducing power, β-carotene, and scavenging of hydrogen peroxide (H2O2). Our results found that EOC represents, respectively (0.064 ± 0.013 and 0.027 ± 00 mg Quer E/100 µL), of flavonoid and flavonol. Then, it exhibited a potential activity of reducing power (at 300 mg/mL, which was found to be 0.82 ± 0.07), β-carotene-linoleic acid (AA% = 69.28 ± 3.5%), and scavenging of H2O2 (IC50 = 0.23 ± 0.008 mg/mL). In vivo, aspirin given to rats at the dose of 600 mg/kg body weight induced histomorphological damage in brain, lung, and intestine. However, our data found that the pretreatment with EOC offered a significant protection against the injury induced by aspirin. It can be concluded that the protective effect of EOC can be due to its antioxidant activities.

scholarly journals A Subpressor Dose of Angiotensin II Elevates Blood Pressure in a Normotensive Rat Model by Oxidative Stress

2015 ◽  
pp. 153-159 ◽  
Author(s):  
M. M. GOVENDER ◽  
A. NADAR
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Mrna Expression ◽  
Rat Model ◽  
Wistar Rat ◽  
Control Group ◽  
Sod Activity ◽  
Male Wistar Rats ◽  
Experimental Group

Oxidative stress is an imbalance between free radicals and antioxidants, and is an important etiological factor in the development of hypertension. Recent experimental evidence suggests that subpressor doses of angiotensin II elevate oxidative stress and blood pressure. We aimed to investigate the oxidative stress related mechanism by which a subpressor dose of angiotensin II induces hypertension in a normotensive rat model. Normotensive male Wistar rats were infused with a subpressor dose of angiotensin II for 28 days. The control group was sham operated and infused with saline only. Plasma angiotensin II and H2O2 levels, whole-blood glutathione peroxidase, and AT-1a, Cu/Zn SOD, and p22phox mRNA expression in the aorta was assessed. Systolic and diastolic blood pressures were elevated in the experimental group. There was no change in angiotensin II levels, but a significant increase in AT-1a mRNA expression was found in the experimental group. mRNA expression of p22phox was increased significantly and Cu/Zn SOD decreased significantly in the experimental group. There was no significant change to the H2O2 and GPx levels. Angiotensin II manipulates the free radical-antioxidant balance in the vasculature by selectively increasing O2− production and decreasing SOD activity and causes an oxidative stress induced elevation in blood pressure in the Wistar rat.

Evaluation of Oxidative Stress potential of some Nsaıds against Hydrogen Peroxide in experimental animal

2021 ◽  
pp. 6194-6200
Author(s):  
KM Diksha Singh ◽  
Vikram Singh ◽  
Adity Singh ◽  
Vipin Kesharwani
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Salicylic Acid ◽  
Liver Steatosis ◽  
Chronic Kidney Failure ◽  
Acetyl Salicylic Acid ◽  
Control Group ◽  
Experimental Protocol ◽  
Examination Result ◽  
Experimental Protocols

Background: Oxidative stress is imbalance between aggressive and defensive system. Overproduction of oxidative stress contribute in pathogenesis of many diseasesincluding Parkinsonism, Alzheimer diseases, apoptosis, hepatic fibrosis ,chronic kidney failure and liver steatosis etc . There are several OTC drugs including NSAIDs that generate oxidative stress when administered. So there is a need to explore about these drugs. Therefore this study was designed to evaluate the oxidative stress potential of Acetaminophen, acetyl salicylic acid and Celecoxib NSAIDs. Objective: The present study is design to investigate the oxidative stress of NSAIDs of acetaminophen, aspirin and Celecoxib drug with reference to the hydrogen peroxide. Material and method: The Experimental protocol was designed for estimate the level of oxidative stress in NSAIDs treated animals against hydrogen peroxides. Animal of control group received only vehicle throughout experimental protocol. Rats of AAP group, ASA group ,CX group were exposed to acetaminophen (150mg/kg; orally) acetyl salicylic acid (300mg/kg ;orally) and Celecoxib (50mg/kg; orally) for forty two days . Rodent of HP group were challenged with Hydrogen peroxides (0.5%) with same schedule as above. At end of experimental protocols, all the animals were sacrificed and their organ were identified and collected for oxidative stress estimation and histological examination. Result: NSAIDs administration caused increase in oxidative stress measured in terms of SOD, CAT, MDA, GSH and GPx. HP administration produced maximum oxidative stress compare to all other groups. Oxidative parameter i.e. SOD, CAT, GSH and GPx were found to be decreased as compare to control rats. However MDA were found to be increased as compare to control rats. Additionally, CX produced less oxidative stress compare to other NDAIDs. Further, histological examinations support the biochemical results. Conclusion: From the above observations it can be concluded that NSAIDs have oxidative stress potential and generate oxidative stress and damage the organs when administrated chronically. Thus, these drugs should be used judiciously.

scholarly journals Protective Effect of Melatonin Against Radiotherapy-Induced Small Intestinal Oxidative Stress: Biochemical Evaluation

Medicina ◽  
2019 ◽  
Vol 55 (6) ◽  
pp. 308 ◽  
Author(s):  
Ahmed Eleojo Musa ◽  
Dheyauldeen Shabeeb ◽  
Haider Saadoon Qasim Alhilfi
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Radical Scavenging ◽  
Common Side Effect ◽  
Control Group ◽  
Intestinal Damage ◽  
Pelvic Malignancies ◽  
Group I ◽  
Male Wistar Rats ◽  
Small Intestinal

Background and Objectives: Radiation enteritis is a common side effect after radiotherapy for abdominal and pelvic malignancies. The aim of the present study was to investigate the protective effect of melatonin, known for its free radical scavenging ability, against radiotherapy-induced small intestinal oxidative damage. Materials and Methods: Thirty male Wistar rats were randomly assigned to six groups (5 rats in each) as follows: Group I (control group) rats received neither radiation nor melatonin; group II rats received only 8 Gy single dose of gamma radiation to their abdomen and pelvis regions; group III (administered with only 50 mg/kg melatonin); group IV (administered with only 100 mg/kg melatonin); group V (50 mg/kg melatonin + 8 Gy radiation), group VI (100 mg/kg melatonin + 8 Gy radiation). All rats were sacrificed after 5 days for biochemical assessments of their intestinal tissues. Results: Treatment with melatonin post irradiation significantly reduced malondialdehyde (MDA) levels as well as increased both superoxide dismutase (SOD) and catalase (CAT) activities of the irradiated intestinal tissues. In addition, melatonin administration with different doses pre irradiation led to protection of the tissues. Moreover, the 100 mg/kg dose was more effective compared to 50 mg/kg. Conclusions: The results of our study suggest that melatonin has a potent protective effect against radiotherapy-induced intestinal damage, by decreasing oxidative stress and increasing antioxidant enzymes. We recommend future clinical trials for more insights.

scholarly journals Protective effect of apricot (Prunus armeniacaL.) on hepatic steatosis and damage induced by carbon tetrachloride in Wistar rats

2009 ◽  
Vol 102 (12) ◽  
pp. 1767-1775 ◽  
Author(s):  
Feral Ozturk ◽  
Mehmet Gul ◽  
Burhan Ates ◽  
I. Cetin Ozturk ◽  
Asli Cetin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Protective Effect ◽  
Hepatic Steatosis ◽  
Wistar Rats ◽  
Liver Steatosis ◽  
Radical Scavenging ◽  
Hepatic Necrosis ◽  
Control Group ◽  
Cytoplasmic Matrix

The present study was planned to investigate the protective effect of 10 % and 20 % apricot-containing feed on carbon tetrachloride (CCl4)-induced hepatic steatosis and damage. Adult male Wistar rats (n42) were divided into six groups of seven each, as follows: control group; CCl4group; CCl4+10 % apricot group; CCl4+20 % apricot group; 10 % apricot group; 20 % apricot group. All apricot groups were fed with 10 % or 20 % apricot-containing feed for 5 months. CCl4injections were applied to the CCl4groups at the dose of 1 mg/kg for 3 d at the end of 5 months. In the CCl4group, vacuolated hepatocytes and hepatic necrosis were seen, especially in the centrilobular area. Hepatocytes showed an oedematous cytoplasmic matrix, large lipid globules and degenerated organelles. The area of liver injury was found significantly decreased with apricot feeding. Malondialdehyde and total glutathione levels and catalase, superoxide dismutase and glutathione peroxidase activities were significantly changed in the CCl4group and indicated increased oxidative stress. Apricot feeding decreased this oxidative stress and ameliorated histological damage. We concluded that apricot feeding had beneficial effects on CCl4-induced liver steatosis and damage probably due to its antioxidant nutrient (β-carotene and vitamin) contents and high radical-scavenging capacity. Dietary intake of apricot can reduce the risk of liver steatosis and damage caused by free radicals.

scholarly journals Role of oxidative stress in hearing impairment in patients with type two diabetes mellitus

2009 ◽  
Vol 123 (9) ◽  
pp. 957-963 ◽  
Author(s):  
İ Aladag ◽  
A Eyibilen ◽  
M Güven ◽  
Ö Atış ◽  
Ü Erkokmaz
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hearing Loss ◽  
Hearing Impairment ◽  
Protein Oxidation ◽  
Serum Levels ◽  
Control Group ◽  
Diabetic Patients ◽  
Enzymatic Antioxidants ◽  
Insulin Dependent Diabetic

AbstractObjective:Although many clinical investigations have found a relationship between hearing loss and diabetes mellitus, the pathophysiology of this effect remains controversial. To date, the mechanisms of hearing loss in diabetic patients have been explained in terms of microangiopathy, neuropathy and encephalopathy. However, many reports indicate that some diabetic complications are associated with oxidative stress related to the diabetes itself. In the present study, we hypothesised that oxidative stress may be a cause of hearing loss in diabetic patients.Methods:The study group comprised non-insulin dependent diabetic patients with no signs of microangiopathy or peripheral neuropathy. The control group comprised sex-, age- and body weight matched, non-diabetic subjects. Auditory function was evaluated using pure tone audiometry and tympanometry. Subjects with normal hearing and sensorineural hearing loss were included in the study, whereas subjects with conductive hearing loss were excluded. Both the study group (n = 63) and the control group (n = 37) were divided into subgroups based on the presence and absence of hearing loss. Oxidative stress was evaluated by measuring serum indicators of protein oxidation and lipid peroxidation, serum levels of nitric oxide and various non-enzymatic antioxidants, and the activity of various enzymatic antioxidants.Results:The non-insulin dependent diabetic patients had significantly higher serum levels of protein oxidation products, nitric oxide, enzymatic antioxidant activity (i.e. glutathione peroxidase and superoxide dismutase), compared with the control group (p < 0.05). When we compared the groups in relation to the presence of hearing loss, the nitric oxide level was significantly increased in the diabetic group with good hearing, compared with diabetic patients with hearing loss (p = 0.014). In the diabetic group, a clear, negative correlation was observed between serum levels of nitric oxide and vitamins C and E, and hearing impairment (r = −0.395,r = −0.318,r = −0.500, respectively). There was also a positive correlation between serum vitamin C concentrations and hearing levels in the control group (r = 0.417).Conclusion:These results suggest that oxidative stress may play an important role in hearing impairment in diabetic patients. In this process, increased protein oxidation appears to be more important than lipid peroxidation. Nitric oxide may have a protective effect on hearing, as may some nonenzymatic antioxidants such as vitamin C and E.

scholarly journals Toxicity evaluation and protective effect of Rhus longipes Engl. leaf extract in paracetamol induced oxidative stress in wister rats

2017 ◽  
Vol 6 (2) ◽  
pp. 73-77
Author(s):  
Olubukola S. Olorunnisola ◽  
◽  
Adewale Adetutu ◽  
Abiodun O. Owoade ◽  
Babatunde T. Adesina ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Protective Effect ◽  
Leaf Extract ◽  
Control Group ◽  
P Value ◽  
Standard Drug ◽  
Test Of Significance ◽  
Dose Dependent ◽  
Isolated Liver

Aim: Acute toxicity and protective effect of ethanol leaf extract of Rhus longipes Engl. against Paracetamol induced oxidative stress was investigated. The LD50 of the leaf extract was determined using up and down technique and the effect of 1/10th and 1/20th/ LD50 of the extract on antioxidants enzymes and non-enzymes were assessed in the serum and isolated liver of normal and Paracetamol intoxicated rats. Data obtained were analyzed by one-way analysis of variance (ANOVA) and Dunnett’s t-test was used as the test of significance. Values were considered significant at P value < 0.05. The results obtained indicated that LD50 of Rhus longipes Engl. leaf extract is greater than 5000 mg/kg /body weight. A significant (p<0.05) increase was observed in the level of hepatic (H) TBARs (81.97%), Catalase (38.42%) and serum (S) TBARs (164.44%) and catalase (64.72%) respectively but, a significant (P<0.05) decrease in hepatic activities of SOD, GPX, GR, vitamin C and E in paracetamol treated groups when compared with the serum and normal control group respectively. The extracts (250 and 500 mg/kg/body/weight) and the standard silymarin significantly (p<0.05) restored the derange antioxidants parameters to near normal in dose dependent manners. The activities of the extract at the highest concentration (500 mg/kg/b.wt) compared favourably with the standard drug. The results suggested that the leaf extract of Rhus longipes Engl. contain bioactive compounds which could protect against toxicity induced oxidative stress. The results of this study can be used as a basis for further investigations in the search for the bioactive principle.

scholarly journals Protective Effect of Combination Commercial Black Seed Oil (Nigella sativa) and Honey Against Cisplatin-Induced Hepatotoxicity in Rats

2020 ◽  
Vol 1 (2) ◽  
pp. 43
Author(s):  
Andri Muhrim Siddiq ◽  
Muhammad In'am Ilmiawan ◽  
Mitra Handini
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Rat Liver ◽  
Liver Tissue ◽  
Seed Oil ◽  
Negative Control Group ◽  
Negative Control ◽  
Control Group ◽  
Black Seed ◽  
Black Seed Oil

Background: The chemotherapeutic use of cisplatin (CP) is restricted because of its hepatotoxicity induced by oxidative stress. Malondialdehyde (MDA) is a secondary product of lipid peroxidation as a biomarker of oxidative stress. Individual administration of black seed oil (BSO) or honey (H) demonstrated hepatoprotective effect in rats. Interaction of both substances when administrated as combination can be evaluated using combination index (CI) to quantitatively depict synergism (CI<1), additive (CI=1) and antagonism effect (CI>1). Objective: to know the combination effect of BSO and honey on rat liver tissue given CP exposure. Methods: This study used 30 rats were divided into 10 groups. Normal group (N); Negative control group (NC); P1-P4 groups were administerated BSO (1 and 2 mL/kg) and honey (3.7 and 7.4 mL/kg); P5-P8 groups were combination of BSO and H. P1-P8 groups were given BSO and honey orally for 21 days. On the 18th day, NC and P1-P8 groups were given CP 8 mg/kg intraperitoneally, while the N group was given NaCl 0.9% 1 mL/kg intraperitoneally. Result: Malondialdehyde (MDA) levels were found to be lower in P1-P8 groups compared to negative control group and P6 and P7 groups have levels equivalent to MDA levels of normal control group (p > 0.05). Conclusion: Combination of BSO and honey provides a protective effect on cisplatin-induced rat liver tissue damage indicated by reduced MDA levels, but all combination group showed antagonism effect.

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