Effect of adalimumab on experimental corneal neovascularization model.

PURPOSE: To evaluate the efficacy of adalimumab (ADA) on inhibition of experimental corneal neovascularization (CNV) and compare the outcomes with bevacizumab (BEVA). METHODS: Twenty-four female Winstar rats (48 eyes) were used. Silver/Potassium Nitrate sticks were used for creating CNV. Forty-eight eyes of the rats were separated into 6 groups. The eyes which only NaCl was injected subconjunctivally (SC) formed Group-1. The eyes which CNV was created and NaCl, BEVA (2.5 mg/0.05 mL), ADA (2.5 mg/0.05 mL), respectively, were injected SC formed group-2, 3 and 4. The eyes which only BEVA and ADA, respectively, were injected SC formed group-5 and 6. Five days later the animals were sacrificed. Hematoxylin and eosin staining, Masson trichrome staining, Vascular endothelial growth factor (VEGF), and Platelet-derived growth factor (PDGF) antibodies were performed. RESULTS: Histochemical results showed that there was no histopathological finding in group-1, 5, and 6. Collagen fiber irregularity was observed in group-2 and there was a significant improvement in collagen fiber irregularity in group-3 and 4. Collagen fiber proliferation was higher in group-2 than in group-3 and 4. VEGF and PDGF stainings were not observed in group-1, 5, and 6. VEGF and PDGF stainings were observed in group-2 and significantly decreased in group-3 and 4 compared to group-2. ADA was found to be superior to BEVA in terms of decreasing VEGF staining. CONCLUSION: Both BEVA and ADA were effective in inhibiting CNV. Subconjunctival ADA seems to be more effective than BEVA in terms of inhibiting VEGF expression. Further experimental studies about ADA and BEVA are needed.

Curcumin induces apoptosis through caspase dependent pathway in human colon carcinoma cells.

BACKGROUND: We investigated the apoptotic effects of curcumin in the colon carcinoma cell line SW480. METHODS AND RESULTS: Cells were treated with 40-200 µM curcumin for 24, 48, and 72 h, and the IC50 values were determined for each time interval. BrdU, caspase-3, and TUNEL staining results and the gene expression of FADD, CASP8, and CASP3 were evaluated. Curcumin treatments significantly inhibited cell proliferation and significantly induced apoptosis for 24, 48, and 72 h. The proportion of BrdU-stained cells in the control groups were 58%, 57% and 61% and 28%, 27%, and 30% in the curcumin treatment groups at 24, 48, and 72 h, respectively. The proportion of apoptotic cells was 28%, 29%, and 28% in the control groups and 59%, 61%, and 60% in the curcumin treatment groups at 24, 48, and 72 h, respectively. As expected, caspase-3 staining also revealed a higher number of apoptotic cells in curcumin treatment groups at 24, 48, and 72 h compared to controls. The proportion of Caspase-3-stained cells in the control groups were 23%, 25%, and 24% and 59%, 60%, and 62% in the curcumin treatment groups at 24, 48, and 72 h, respectively. To prove caspase-3 staining results, FADD, CASP8, and CASP3 gene expressions were evaluated by real-time qPCR. Unlike the immunohistochemical results, no statistically significant upregulation was found at 24 and 48 h, while relative gene expressions of FADD, CASP8, and CASP3 was significantly upregulated at 72 h. The expression level increase was 0.88-, 1.19-, and 2.11-fold for FADD, 1.25-, 1.29-, and 1.59-fold for CASP8, and 1.33-, 1.46-, and 3.00-fold for CASP3 at 24, 48, and 72 h, respectively. CONCLUSIONS: These results suggest that curcumin may be a potential protective or treatment agent against colon cancer; however, further studies on curcumin-rich diets and curcumin bioavailability are required.

Protective effects of resveratrol and avocado oil against paracetamol-induced hepatotoxicity in rats.

This study sought to assess the protective effects of resveratrol and avocado oil in relation to paracetamol-induced hepatotoxicity in rats. The rats were divided into five groups, namely the control, paracetamol (600 mg/kg), resveratrol (RES; 10 mg/kg) + paracetamol, avocado oil (AVO; 200 mg/kg) + paracetamol, and RES + AVO + paracetamol groups. The hepatoprotective activity was evaluated by measuring biochemical parameters such as the total antioxidant status (TAS) and the total oxidant status (TOS) in each rat's liver homogenates. Any DNA damage was assessed by means of a comet assay. The results showed that the TOS levels were significantly increased in the paracetamol group when compared with the control group. The TOS levels were found to be significantly lower in the paracetamol groups, in comparison with the RES, AVO, and RES + AVO groups. Moreover, the TAS levels significantly increased in the RES and RES + AVO groups when compared with the paracetamol group. The histopathological examination revealed necrotic areas in the rats' livers. Pretreatment with both RES and RES + AVO was found to reverse the oxidative stress parameters, DNA damage, and necrosis induced by paracetamol. These results suggest that a combination of REV and AVO may protect against paracetamol-induced hepatotoxicity due to their antioxidant properties.

A study on Wistar Albino rats: investigating protective role of ramelteon on liver damage caused by methotrexate.

Methotrexate is an important immunosuppressive and antineoplastic drug and is widely used for treatment. However, hepatotoxicity is one of the major adverse effects of methotrexate. In this study, it was aimed to investigate whether ramelteon has a possible protective effect on hepatotoxicity induced by methotrexate. Thirty-two Wistar albino rats were equally divided into four groups: control, methotrexate, methotrexate + ramelteon, and ramelteon. Following a single dose of 20 mg/kg, methotrexate (i.p.), either saline or ramelteon 10 mg/kg (orally) was administered for 7 days. After treatment, animals were sacrificed, and histopathological analyses were evaluated with Hematoxylin-eosin (H-E), immunohistological analyses were evaluated with Interleukin-1 Beta (IL-1ß) and Caspase 3 (CAS-3), biochemical analyzes were evaluated with Total Oxidant Status (TOS), Total antioxidants status (TAS), Oxidative Stress Index (OSI), aspartate aminotransferase (AST), alanine aminotransferase (ALT) activities, at last genetical analyses were evaluated with Sirtuin-1 (SIRT-1) - P53 gene expressions. In the control and ramelteon groups, normal histological structures were observed, while histopathological findings were observed in the methotrexate group. Increasing levels of IL-1ß staining, CAS-3 staining, p53 gene expression, TOS, OSI, AST and ALT were observed in methotrexate group while were observed decreasing levels of TAS and SIRT-1 gene expression (p < 0.05). However, ramelteon reduced the increased findings in methotrexate-induced hepatotoxicity (p < 0.05). The results of the present study showed that ramelteon protects against methotrexate induced hepatotoxicity in rats via SIRT-1 signaling by histological, immunohistological, biochemical and genetical analyses.

Does Boric Acid Inhibit Cell Proliferation on MCF-7 and MDA-MB-231 Cells in Monolayer and Spheroid Cultures by Using Apoptosis Pathways?

Most breast cancers originate in the lobules or ducts of the breast. Breast cancer as the second main cause of death among women in the world is the most common kind of cancer in women. Studies have been conducted to find the optimal treatment for breast cancer. Moreover, the therapeutic effects of different drugs and substances on this disease have been intensively researched. Boric acid accounts for 96% of the boron content in body fluids, and its derivatives are absorbed by the human body. It is assumed to be represented as (B(OH)2). Experimental studies have shown a reduction of cell proliferation and stimulation of apoptosis in some melanoma, prostate, and colon cancer cell lines through boric acid. The aim of this study was to investigate if boric acid could be used for treating breast cancer. The impacts of boric acid on the human breast carcinoma cell lines MCF-7 and MDA-MB-231 were studied with TUNEL, BrdU, caspase-3, and endo-G immunohistochemical studies in 3D and 2D culture systems. Furthermore, we conducted a qRT-PCR study to show changes in the expression of some genes involved in apoptosis. Suppression of cell proliferation through boric acid-inducing apoptosis was observed both in 3D and 2D culture conditions. These results are compatible with the gene expression results. The ENDOG, CASP3, CASP8, and CASP9 gene expression significantly changed at all time intervals in MCF-7 and MD-MB-231 cell lines boric acid can potentially treat breast cancer as an anti-cancer agent candidate.

Linalool prevents kidney damage by inhibiting rifampicin-induced oxidative stress and apoptosis.

Today, kidney diseases are increasing day by day and life quality is decreasing. In hospitalized patients of all ages, acute kidney injury (AKI) is commonly observed and associated with high rates of morbidity and mortality. Rifampicin (RF) or rifampin is an antibiotic drug from the rifamycin group with a bactericidal effect. RF causes acute kidney injury, often anemia, thrombocytopenia, liver damage and side effect such as cell death. RF causes tissue damage by means of oxidative stress and apoptosis. Thus, in this study, it was examined whether linalool (LN) which had antinociceptive, antimicrobial, antioxidant and anti-inflammatory effects, was beneficial for kidney damage in order to eliminate the side effects of RF. NGAL mRNA, creatinine (Cr), blood urea nitrogen (BUN), Caspase 9 (CAS-9) and nuclear factor-κB (NF-κB) levels increased in the group treated with RF compared to the control group, while the levels of albumin, uric acid and total protein were decreased in the RF-treated group. NGAL mRNA, BUN, Cr, CAS-9 and NF-κB levels decreased significantly in RF+LN administered rats, while it was observed that there was an increase in the levels of albumin, uric acid and total protein. From the results obtained, it was observed that LN was determined to be very effective in preventing tissue damage in kidneys caused by oxidative stress by RF.

Apoptotic effects of Phlomis armeniaca mediated biosynthesized silver nanoparticles in monolayer (2D) and spheroid (3D) cultures of human breast cancer cell lines.

The purpose of current research was to assess the apoptotic effects of biofabrication silver nanoparticles (AgNPs) mediated by the aqueous extract of Phlomis armeniaca on human breast cancer cells (MCF-7 and MDA-MB-231) in monolayer (2D) and spheroid (3D) cultures. The biosynthesized AgNPs were characterized by UV-Vis spectrophotometer (the peaks of resonances at 432 nm), scanning electron microscopy (SEM) and energy-dispersive X-ray spectrometry (EDS). 1-20 µM/mL AgNPs were applied to MCF-7 and MDA-MB-231 cell lines to determine IC50 values at 24, 48 and 72nd h and were found to be 10 µM/mL for both cell lines. Immunohistochemical staining results of BrdU, TUNEL, caspase-3 and Endo G in both 2D and 3D cultures and gene expression levels of caspases (caspase-3, -8 and -9) and Endo G were evaluated. Moreover, the total oxidant/antioxidant status (TOS-TAS) due to AgNPs application in both cell culture mediums was evaluated. AgNPs treatment results in both cell lines in both 2D and 3D cultures showed a significant decrease in the BrdU labeling index, while large amounts of cells were labelled with TUNEL and Endo G. In 2D culture, Endo G expression increased in MCF-7 cells at 48 and 72nd hours, while it increased significantly in MDA-MB-231 cells at all hours. OSI results show that ROS production is increased in cell medium treated with AgNPs. In conclusion, AgNPs mediated by Phlomis armeniaca, synthesized by a green method, successfully induced damage to mitochondria, resulting in cell cycle arrest and consequent cell proliferation blockade and death in both MCF-7 and MDA-MB-231 cells.

Thymoquinone ameliorates amikacin induced oxidative damage in rat brain tissue.

We investigated the potential neuroprotective effects of thymoquinone (TQ) on amikacin (AK) induced oxidative damage in rat brain. We used 21 male rats divided randomly into three equal groups. The control group was injected intraperitoneally (i.p.) with 0.5 ml 0.9% aqueous NaCl and given 1 ml 0.9% aqueous NaCl orally. The AK group was administered 1.2 g/kg aqueous AK i.p. as a single dose on the day 3 of the study. The AK + TQ group was given a single 1.2 g/kg dose of AK i.p. on the day 3 of the study plus 40 mg/kg/day TQ by oral gavage daily. Treatment with TQ increased serum ferritin and decreased serum calcium levels significantly. TQ also decreased NADPH oxidase-2, NADPH oxidase-4, and caspase-3 levels. Decreased malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) and catalase (CAT) activities were detected in the AK + TQ group compared to the AK group. TQ administration inhibited lipid peroxide formation and blocked oxidative reactions, which reduced the MDA level and increased SOD and CAT activities induced by AK. Oxidative damage caused by AK was ameliorated by TQ treatment owing to its antioxidative and anti-apoptotic effects. TQ may be a potential therapeutic agent for reducing the severity of AK induced oxidative damage to the brain.

Boric acid suppresses cell proliferation by TNF signaling pathway mediated apoptosis in SW-480 human colon cancer line.

BACKGROUND/AIM: Colon cancer is one of the most common cancers. Treatment success and survival rates are not high enough with current approaches. Therefore, there is a need to develop new agents and treatment methods. Boric acid is the most frequently observed form of boron. Some epidemiological data suggest that environmental exposure to boric acid reduces the incidence of prostate cancer in men, cervical and lung cancers in women. Experimental studies show, boric acid reduces cell proliferation and stimulates apoptosis in some prostate, melanoma, breast cancer cell lines. In this study, it was investigated whether boric acid could be a new candidate molecule that could be used in the treatment of colon cancer. MATERIALS AND METHODS: The effects of boric acid on human colon adenocarcinoma cell line SW-480 were investigated with BrdU, TUNEL, Caspase-3, and AIF immunohistochemical studies in both 2D and 3D culture systems. In addition, a qRT-PCR study was carried out to determine the expression changes in key genes that take part in apoptosis. RESULTS: We observed that boric acid suppresses cell proliferation and induces apoptosis both in 2D and 3D culture conditions. In addition, as a result of qRt-PCR studies, it was revealed that the observed apoptotic process was related to the TNF signaling pathway. CONCLUSION: Boric acid can be considered as a potential anti-cancer agent candidate for colon cancer treatment. DATA AVAILABILITY: All data generated or analyzed during this study are included in this published article.

Is Quercetin Beneficial for Colon Cancer? A Cell Culture Study, Using the Apoptosis Pathways.

BACKGROUND: Quercetin (QCT) is a dietary flavonoid with many beneficial effects (e.g., antioxidant, antiaging, antidiabetic, antifungal effects, and regulation of gastrointestinal motor activity in human); furthermore, it induces apoptosis, cell cycle arrest, and differentiation. OBJECTIVE: The apoptotic effects of OCT were investigated on SW480 human colon cancer cell lines in monolayer and spheroid cultures. METHODS: Quercetin (40-200 µM) was applied, and Inhibitory Concentration (IC50) doses were determined for three time intervals (24, 48, and 72 h). The effective dose was determined and applied for analyses, including staining with BrdU to investigate cell proliferation, terminal deoxynucleotidyl transferase dUTP nick and labeling (TUNEL) to investigate apoptosis, and caspase-3 and Apoptosis Inducing Factor (AIF) to investigate caspase-dependent or independent apoptotic pathways. RESULTS: The effective dose of QCT was determined to be 200 µM and was found to induce apoptosis and inhibit cell proliferation at 24, 48, and 72 h,both in 2D and 3D cultures. Significant increases were observed in both caspase-3 and AIF staining, but cells showed greater caspase-3 staining compared with AIF staining at all time intervals (p<0.05). CONCLUSION: The QCT treatment groups showed more cell death and less cell growth compared with the untreated control groups in both 2D and 3D cultures of SW480 cell lines. The results suggest that quercetin induces apoptosis, inhibits cell proliferation, and has a protective role against colon cancer. However, further studies are needed to clarify its mechanism of action.

Secoisolariciresinol diglucoside induces caspase-3-mediated apoptosis in monolayer and spheroid cultures of human colon carcinoma cells.

Apoptotic effects of secoisolariciresinol diglucoside (SDG) in 2D and 3D cultures of SW480 cells were investigated. 40-200 µM SDG was used and IC50 values were determined for three different time intervals as 24, 48, or 72 hr for further experiments. BrdU, TUNEL, AIF, and caspase-3 stainings were used. SDG inhibited cell proliferation almost half and half for all time intervals in 2D and 3D cultures and also, induced apoptosis. Apoptotic cell percentages in the control group for 24, 48, and 72 hr were 27.00%, 29.00%, and 28.00%, respectively, while in the SDG treatment group were 59.00%, 61.00%, and 62.00%, respectively. In the spheroid cell culture, apoptotic cell percentages in the control group for 24, 48, and 72 hr were 6.90%, 7.20%, and 7.10%, respectively, while in the SDG treatment group were 19.50%, 19.50%, and 20.70%, respectively. Caspase-3 and AIF antibodies were used to indicate caspase-dependent and -independent apoptotic pathways. Significant increases were seen in both AIF and caspase-3 stainings when compared to the control group but caspase-3 staining results were significantly greater when compared to the AIF staining at all time intervals (p < .05). To prove this, CASP3 gene expression was evaluated by RT-qPCR. Unlike staining results, there was no statistically significant change at 24 hr in 2D and 3D cultures. But, significant upregulation at 48 (2.32-fold in 2D and 2.46-fold in 3D) and 72 hr (5.04-fold in 2D and 6.45-fold in 3D) were seen. PRACTICAL APPLICATIONS: Colon cancer is one of the most prevalent cancer in the developed countries and its etiology is complex. Although the underlying mechanisms are mostly unknown, the link between diet and colon cancer is known and dietary habits can promote cancer or protect against it. In recent years, flaxseed is accepted as a significant functional food ingredient and feeding with it could help in to prevent cancer. Secoisolariciresinol diglucoside is a flaxseed lignan and is metabolized to mammalian lignans by the gut. In the present study, SDG was evaluated for its apoptotic effects in colon carcinoma cell line via monolayer and spheroid cultures using immunohistochemical and gene expression techniques. Findings of this study suggest that SDG may protect against cancers and in particularly against colon cancer and further investigations has to be carried out for detailed underlying mechanisms.

DNA damage effect of cyprodinil and thiacloprid in adult zebrafish gills.

Cyprodinil and thiacloprid are two of the most commonly used pesticides in Turkey. It is more likely to reach humans or animals due to their widespread use. This study aims to investigate whether there is a DNA damage risk due to cyprodinil and thiacloprid exposure. Zebrafish, which is used as a model organism in health and environmental research, and comet assay were chosen to demonstrate this damage. Ten zebrafish per group were exposed to 2 different concentrations for each pesticides (0.31 and 0.155 mg/L for cyprodinil and 1.64 and 0.82 mg/L for thiacloprid) for 21 days. After, gills were excised and comet assay was performed. Photos of an average of 50 cells per slide were taken and were analyzed with visual evaluation program. DNA damage was found to be increased in the 0.31 mg/L cyprodinil, 0.82 mg/L thiacloprid, and 1.64 mg/L thiacloprid treatment groups when compared to the control group (p < 0.001). Average tail DNA percentage parameter values were 9.45 ± 0.51, 10.30 ± 0.34, 11.17 ± 0.33, and 2.47 ± 0.06 respectively. Cyprodinil and thiacloprid were identified as genotoxic agents that should be investigated further.

Evaluation of the effects of vitamins C and E on experimental orthodontic tooth movement.

Background. This experimental study aimed to assess the effects of Vitamins C and E on orthodontic tooth movement. Methods. Fifty-one male Wistar albino rats were divided into six groups: five appliance groups and one control group. The appliance groups had an orthodontic appliance consisting of a closed-coil spring ligated between the maxillary incisor and maxillary first molar (50 g). Vitamin E and C (150 mg/kg) were injected intraperitoneally per day in the first and second groups, respectively. Vitamins E and C (20 µL) were locally injected into the periodontal gap of the moving teeth in the third and fourth groups, respectively, once every three days. No vitamin was injected in the last (fifth) appliance group.The experimental period was 18 days. Histological and biochemical (alkaline phosphatase, osteocalcin, and NTx levels) evaluations of the samples were performed, and maxillary incisor‒molar distance was measured before and after the experiment. Results. The amount of tooth movement was similar in the appliance groups. All the vitamin groups showed significantly increased osteoblastic activity, while those treated with systemic vitamins exhibited significantly increased numbers of collagen fibers on the tension side compared to the appliance control group (P<0.05). Conclusion. Vitamin C and E supplements positively affected bone formation on the tension side of the teeth during experimental orthodontic tooth movement.

Investigation of apoptotic effect of juglone on CCL-228-SW 480 colon cancer cell line.

BACKGROUND: Colon cancer is a major cause of morbidity and mortality in the world. Juglone is a natural compound which has been isolated from Juglans mandshurica Maxim, and it has various pharmacological effects such as antiviral, antibacterial, and anticancer. In our study, we aimed to investigate the effect of juglone on CCL-228-SW 480 colon carcinoma cell line in monolayer and spheroid culture medium. MATERIALS AND METHODS: The CCL-228-SW 480 cell lines were cultured in both monolayer and spheroid cultures. Cells were treated with juglone at 24, 48, and 72 h of incubation. ID50 inhibition was determined on the dose for juglone and after it was found 20 µM was applied to the cells to examine the effect of juglone on CCL-228-SW 480 colon carcinoma cell line. After Juglone was applied the BrdU marking index, Transferase dUTP Nick ends Labeling (TUNEL) assay, active caspase-3 assay, apoptosis-inducing factor (AIF) assay were determined by immunohistochemistry in both the monolayer and spheroid cultures. RESULTS: The control group had a healthy pattern of S-phase fraction, and many of the CCL-228-SW 480 cells nuclei were observed to be positive for BrdU. Terminal Deoxynucleotidyl TUNEL-positive cells, active Caspase-3, and AIF were detected after treatment with juglone in both the monolayer and spheroid cultures. CONCLUSIONS: The dead cell count was higher in the CCL-228-SW 480 cell lines with juglone applied than in the controls. Juglone significantly inhibits the proliferation and induces the apoptosis of CCL-228-SW 480 cells in vitro.

Determination of Apoptotic Effect of Juglone on Human Bladder Cancer TCC-SUP and RT-4 Cells: An In Vitro Study.

This study aimed to investigate the effects of juglone on the human bladder carcinoma cell lines TCC-SUB and RT-4 in monolayer and spheroid cultures. Cells were treated with juglone at 24, 48, and 72 h of incubation. The activity of caspase-3 was detected in vitro using a caspase-3 colorimetric assay kit according to the manufacturer's instructions. The bromodeoxyuridine (BrdU) labeling index was used to determine the cells of the synthesis phase. The terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay was used to determine the death of cells in both the monolayer and spheroid cultures. The control group had a large S-phase fraction and many of the TCC-SUB and RT-4 cells nuclei were observed to be positive for BrdU. The dead cell count was higher in the TCC-SUB and RT-4 cell lines with juglone applied than in the controls. We conclude that juglone significantly inhibits the proliferation and induces the apoptosis of TCC-SUB and RT-4 cells in vitro.

The protective effect of pomegranate juice in paracetamol-induced acute hepatotoxicity in rats.

AIM: Being the most commonly used antipyretic and analgesic, paracetamol is one of the most common causes of childhood poisoning in the world and maintains its importance also in our country. Paracetamol poisoning is one of the most common causes of liver failure. This study aimed to investigate if pomegranate juice had protective effect in acute liver toxicity related with paracetamol. MATERIAL AND METHODS: A total of 36 Wistar-Albino rats were divided into four groups as the paracetamol group (3 000 mg/kg paracetamol), the pomegranate juice + paracetamol group (1.5 mL pomegranate juice plus 3 000 mg/kg paracetamol), the pomegranate juice group (1.5 mL pomegranate juice) and the control group (1.5 mL distilled water). Pomegranate juice and distilled water were administered for eight days. Paracetamol was administered on day 8. The level of thiobarbituric acid reactive substances, as an oxidative marker, was measured in the blood and liver tissue on day 9. In addition, liver tissues were evaluated histologically (in terms of increased connective tissue, granular degeneration, mononuclear cell infiltration, necrotic cells and vascular congestion). RESULTS: The liver tissue and blood thiobarbituric acid reactive substances levels were found to be significantly lower in the pomegranate juice + paracetamol group compared to the paracetamol group (p<0.05). Histologically, structural changes related with damage were observed in both the paracetamol group and pomegranate juice + paracetamol group. The extent of damage was statistically significantly lower in the pomegranate juice + paracetamol group (p<0.001). CONCLUSIONS: Our results related with oxidative and histologic evaluation showed that pomegranate juice might have a preventive effect in paracetamol-induced acute liver damage.

The protective effect of Capparis ovata in acute hepatotoxicity induced by paracetamol.

BACKGROUND/AIM: To investigate the efficiency of Capparis ovata as a protective agent against acute paracetamol toxicity of the liver. MATERIALS AND METHODS: A total of 36 Wistar albino rats were divided into 4 groups: 1) paracetamol, 2) Capparis ovata + paracetamol, 3) Capparis ovata, and 4) control. Groups 2 and 3 were given Capparis ovata and Groups 1 and 4 distilled water for 8 days. On day 8, 3000 mg kg-1 paracetamol was administered orally to Groups 1 and 2. Samples were taken on day 9. AST, ALT, total bilirubin, direct bilirubin, GGT, and ALP levels were assessed. Lipid peroxidation markers and thiobarbituric acid-reactive substance (TBARS) levels were measured in the blood and liver. Liver tissues were evaluated histologically. RESULTS: AST, ALT, and total bilirubin levels were lower in Group 2 than in Group 1 (P < 0.05). TBARS levels were lower in Groups 2 (P = 0.000), 3 (P = 0.001), and 4 (P = 0.001) than in Group 1. Degenerative findings were lower in the Capparis ovata + paracetamol group than in the paracetamol group (P < 0.05). CONCLUSION: It can be concluded that Capparis ovata has a protective effect on the liver, both histopathologically and biochemically, against paracetamol-induced liver injury.