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Ellagic acid (EA) has protective effect on testicular damage and this natural compound decreases oxidative damage. The present study aims to examine the preventive effect of ellagic acid (EA) against carbon tetrachloride (CCl 4 )-induced testicular tissue damage in rats. In testicular tissue, tumor necrosis factor-α (TNF-α), Nuclear factor erythroid-2 related factor 2 (Nrf-2), B-cell lymphoma-2 (Bcl-2), vascular endothelial growth factor (VEGF), Nuclear factor-kappa B (NF-κB), cysteine aspartic proteases (caspase-3) and protein kinase B (Akt) synthesis levels were analyzed by western blot method, reactive oxygen species (ROS) was measured by malondialdehyde (MDA) levels, Glutathione (GSH) level and catalase (CAT) by spectrophotometer. As a result, in comparison with the CCl 4 group, caspase-3 and Nrf-2 protein synthesis levels increased in EA + CCl 4 group, however, VEGF, Bcl-2, NF-κB, TNF-α and Akt protein synthesis levels decreased, EA application raised GSH levels and CAT activity, reduced MDA levels. In this study, in silico tools were applied to confirm the activity of EA against the cancer with macromolecules such as the above mentioned transcription factors. EA, turned out to show significant activity similarly to some cocrystal ligands, particularly against cancer. These results points out that EA can be used as a testicular damage cure drug in future.

Objective: The aim of this study was to evaluate the potential effect of ellagic acid (EA) in the treatment of pancreatic injury. EA has been found to have strong anti-inflammatory, antioxidative, and anticancer properties. The effects of EA on pancreati˜c star cell (PSC) activation and cell functions have been evaluated and it has been shown that it inhibits the activation of basic cell functions and PSCs and . it has antidiabetic activity through its effect on β-pancreas cells., Materials and Methods: In this work, 36 Wistar albino rats ( n  = 36, 8 weeks old) were used. Rats were divided to 4 groups and 9 rats were each group. Groups: Group 1: control group; Group 2: EA group; Group 3: carbon tetrachloride (CCl 4 ) group; Group 4: EA + CCl 4 group. Animals were decapitated after 8 weeks and their pancreas tissue samples were taken and researched. In pancreas tissue, NF-κB, TNF-α, Nrf-2, VEGF, Bcl-2, caspase-3, and Akt proteins expression ratios were analyzed by western blotting method, CAT activity and GSH levels were determined by spectrophotometer and ROS production was detected by MDA., Results: In our results, the Nrf-2 and caspase-3 protein expressions, catalase activities and GSH levels increased, TNF-α, NF-κB, Bcl-2, VEGF, and Akt protein expressions and MDA levels reduced in EA + CCl 4 group comparable to the CCl 4 group., Conclusions: These findings reveal that EA decreases pancreas tissue injury in rats and that EA may also be used as a drug against pancreas tissue injury in the future.

Phytochemicals, bioactive food compounds, found in plants have been described as protective agents against renal injury. This work was planned to evaluate the effects of EA on anti-oxidative and anti-inflammation pathways in kidney damage induced with carbon tetrachloride. In this study, experimental animals (n = 36, 8 weeks old rats) were divided into 4 groups as follows: 1) Control group 2) EA group (10 mg/kg body weight) 3) CCl 4 group (1.5 ml/kg, body weight) 4) EA + CCl 4 group. The potentially protective effect of EA on kidney damage exposed by CCl 4 in rats were evaluated. EA administration protects CCl 4 induced kidney damage against oxidative stress through its antioxidant protection. Treatment of EA significantly reduced lipid peroxidation and improved glutathione and catalase enzyme activity. Recently studies showed that EA activated caspase-3 and nuclear transcription factor erythroid 2 related factor driven antioxidant signal pathway and protected the kidney against damage induced by oxidative stress. Furthermore, EA also markedly decreased the level of cyclooxygenase-2, the vascular endothelial growth factor and tumor necrosis factor-alpha and suppressed the protein synthesis of nuclear factor-kappa-B. This study reveals that EA has kidney protective effect against CCl 4 induced oxidative damage and inflammation.

The aim of this study was to investigate the neuroprotective role of ellagic acid (EA) on CCl 4 -induced brain injury in rats. In this study, the rats were divided into four groups. Groups: (1) Control group; (2) EA group; (3) CCl 4 group; (4) EA + CCl 4 group. In brain tissue, tumor necrosis factor-α (TNF-α), nuclear factor kappa b (NF-kB), cyclooxygenase-2 (COX-2), nuclear erythroid related factor 2 (Nrf-2), cysteine-aspartic acid protease (caspase-3), VEGF (vascular endothelial growth factor) and B-cell lymphoma-2 (bcl-2) protein expression levels were analyzed by western blotting. MDA (malondialdehyde), catalase enzyme activity (CAT) and glutathione (GSH) analysis were determined by spectrophotometer. In our findings, EA ameliorated Nrf-2 and caspase-3 protein expression levels, GSH and catalase activities, NF-kB, TNF-α, VEGF, Bcl-2, COX-2 protein expression levels and MDA levels in CCl 4 intoxicated rats. These results suggest that EA demonstrated the neuroprotective effect on CCl 4 -induced brain damage in rats. PRACTICAL APPLICATIONS: Ellagic acid has different biological activities, these are; antioxidant, anti-inflammatory, antidepressant, antifibrosis, anticancer, neuroprotective and hepatoprotective. For example it was reported that EA protects the cells against DNA injury induced by free radicals and it can prevent the traumatic brain injury. These results obtained from this study reveals that EA has a protective effect against rat brain damage and it may be used as an alternative drugs for the brain injury treatment in future., (© 2020 Wiley Periodicals, Inc.)

The goal of this study was to determine the protective role of ellagic acid (EA) against CCl 4 -induced muscle injury in rats. In this study, 36 Wistar albino rats (n = 36, 8 weeks old) were used. The rats were divided into 4 groups and 9 rats were included each group. Groups: (i) control Group: standard diet; (ii) EA Group: standard diet + EA group; (iii) CCl 4 group: standard diet + CCl 4 group; (iv) EA + CCl 4 group: standard diet + EA + CCl 4 . The animals were decapitated after 8 weeks, and their muscle tissues were received and investigated. In the muscle tissue, TNF-α, COX-2, Nrf-2, NF-kB, caspase-3 and bcl-2 expression levels were analyzed by the western blotting technique, lipid peroxidation was detected by MDA (malondialdehyde), and catalase and GSH levels were determined by a spectrophotometer. In our findings, in comparison to the CCl 4 group, in the EA + CCl 4 group, the Nrf-2 and caspase-3 protein expression levels, GSH and catalase activities increased, while the NF-kB, bcl-2, TNF-α and COX-2 protein expression levels and MDA levels decreased. These results suggest that EA reduces muscle tissue damage rate in rats and that EA may also be used as a potential drug to protect against muscle tissue damage in the future.

Phytochemicals is considered one of the most effective and safe alternative therapy against oxidative linked lung diseases. Ellagic acid (EA), an important component of fruits, nuts, and vegetables, are partly responsible for their beneficial health effects against oxidation-related diseases. In the present study, we investigated the ameliorative effect of EA on lung damage induced by carbon tetrachloride (CCl 4 ) in Wistar male albino rats. Thirty-six male rats (n = 36, 8-week old) were divided into 4 groups, each with 9 rats. The groups were: Control group: received standard diet; EA group: administered with EA (10 mg/kg body weight, intraperitoneal); CCl 4 group: administered with CCl 4 (1.5 mg/kg body weight, intraperitoneal); EA+CCl 4 group: administered with EA and CCl 4 . . The rats were decapitated at the end of experimental period of 8 weeks and the lung tissues were examined. CCl 4 -induced rats showed elevation in the expressions of inflammatory proteins, nuclear factor kappa b (NF-κB), cyclooxygenase-2 (COX-2), and pro-inflammatory cytokine, tumor necrosis factor alpha (TNF-α); and the indicator of lipid peroxidation, malondialdehyde (MDA). Intraperitoneal administration of EA significantly reduced the levels of these markers. EA administration increased the protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf-2) and enhanced the activity of glutathione (GSH) and catalase enzyme (CAT). In addition, EA administration increased the expression levels of the executioner protein of apoptosis, caspase-3, and decreasing pro-survival protein, B cell lymphoma-2 (Bcl-2). In conclusion, these results establishes the protective role of EA in the treatment of lung damage and that in the future, this may have the potential to be used as a medication for the prevention or attenuation of lung diseases. Graphical abstract.