Gentamicin, an aminoglycoside antibiotic, is nowadays widely used in the treatment of gram-negative microorganisms. The antimicrobial, anti-inflammatory, and antioxidant activities of eucalyptol, a type of saturated monoterpene, have been reported in many studies. The aim of this study was to examine the possible effects of eucalyptol on gentamicin-induced renal toxicity. A total of 32 rats were divided into 4 groups; Control (C), Eucalyptol (EUC), Gentamicin (GEN), and Gentamicin + Eucalyptol (GEN + EUC). In order to induce renal toxicity, 100 mg/kg gentamicin was administered intraperitoneally (i.p.) for 10 consecutive days in the GEN and GEN + EUC groups. EUC and GEN + EUC groups were given 100 mg/kg orally of eucalyptol for 10 consecutive days. Afterwards, rats were euthanized and samples were taken and subjected to histopathological, biochemical, immunohistochemical, and real-time PCR examinations. The blood urea nitrogen (BUN) and creatinine (CRE) levels were significantly decreased in the GEN + EUC group (0.76 and 0.69 fold, respectively) compared to the GEN group. The glutathione peroxidase (GPx) and and catalase (CAT) activities were significantly increased in the GEN + EUC group (1.35 and 2.67 fold, respectively) compared to the GEN group. In GEN group, Nuclear factor kappa B (NF-kB), Interleukin 1-beta (IL-1β), Inducible nitric oxide synthase (iNOS), Tumor necrosis factor-α (TNF-α), Caspase-3, 8-Hydroxy-2'-deoxyguanosine (8-OHdG) and Nuclear factor erythroid 2-related factor (Nrf2) expression levels were found to be quite irregular. GEN + EUC group decreased the expressions of NF-kB, IL-1β, iNOS, TNF-α, Caspase-3, and 8-OHdG (0.55, 0.67, 0.54, 0.54, 0.63 and 0.67 fold, respectively), while it caused increased expression of Nrf2 (3.1 fold). In addition, eucalyptol treatment ameliorated the histopathological changes that occurred with gentamicin. The results of our study show that eucalyptol has anti-inflammatory, antioxidative, antiapoptotic, nephroprotective, and curative effects on gentamicin-induced nephrotoxicity.

Eucalyptol (1,8-cineole), a terpenoid oxide, is known as the main component of eucalyptus essential oils. The antimicrobial, anti-inflammatory and antioxidant activities of eucalyptol have been reported in many studies. We investigated the possible effects of eucalyptol (EUC) against hepatotoxicity induced by cisplatin (CIS) in Wistar albino rats. A total of 24 rats were divided into 4 equal groups; Control (C), Eucalyptol (EUC), Cisplatin (CIS), and Cisplatin + Eucalyptol (CIS + EUC). CIS and CIS + EUC groups received cisplatin (12 mg/kg, in a single dose, intraperitoneally (i.p.)). EUC and CIS + EUC groups were treated with eucalyptol (100 mg/kg, seven days, orally). The rats were euthanised under appropriate conditions, and samples were taken. Histopathologically, hepatocyte degeneration and necrosis, sinusoidal dilatation, inflammatory cell infiltration and bile duct proliferation were significantly irregular in the CIS group compared to the C group. However, EUC treatment modulated changes in group CIS. Biochemically, EUC (100 mg/kg) treatment reduced oxidative stress against increased liver hepatotoxicity by decreasing MDA levels and increasing Glutathione (GSH), Glucose-6-phosphate dehydrogenase (G6PD) and Catalase (CAT) levels. EUC treatment down-regulated 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, resulting in reductions DNA damage. It also significantly down-regulated inducible nitric oxide synthase (iNOS) expression. In conclusion, eucalyptol exerts protective effects on cisplatin-induced experimental liver toxicity in rats by improving oxidative stress and oxidative DNA damage and iNOS expressions.

This study was aimed to explore the therapeutic effect of eucalyptol on cisplatin induced kidney damage in Wistar albino rats. The animals were divided into four groups: sham (S), eucalyptol (E), cisplatin (C), and cisplatin + eucalyptol (CE) randomly, six animals in each group. Groups C and CE were received cisplatin (12 mg/kg, a single dose, intraperitoneally (i.p.)). Groups E and CE were treated with eucalyptol (100 mg/kg, for seven days, orally). The blood samples and kidney tissues were collected following sacrification and analyzed histopathologically and biochemically. Histopathological results revealed tubular degeneration and necrosis, inflammatory cell infiltration, tubular lumen dilatation, enlargement of bowman’s space and hyaline cast were significantly irregular in the group C than group S. However, eucalyptol treatment (CE) modulated the alterations in the group C. Serum levels of blood urea nitrogen (BUN) and creatinine (CRE) were considerably higher in the group C compared to the other groups. There was no significant difference among the other groups statistically (except group C) in terms of BUN and CRE values. Eucalyptol treatment (at 100 mg/kg, for seven days) decreased the cisplatin induced increase in serum BUN and CRE levels and restored the reduced Vit C level and CAT activity of kidneys caused by cisplatin. Thus, eucalyptol’s antioxidative, nephroprotective, and curative effects indicated the potential for future drug development.

This study aimed to investigate the effects of Tarantula cubensis alcohol extract (TCAE, Theranekron) and Sorafenib (S) treatments on carcinogenesis, apoptosis and biochemical profile of rats with experimentally induced hepatocellular carcinoma (HCC). In the presented study, 58 male rats were divided into 7 groups; Negative Control (NC, n = 6), NC + TCAE (NCT, n = 6), NC + Sorafenib (NCS, n = 6), Positive Control (PC, n = 10), Positive Control + TCAE (PCT, n = 10), Positive Control + Sorafenib (PCS, n = 10), Positive Control + TCAE + Sorafenib (PCTS, n = 10). The active ingredients Diethylnitrosamine (DEN, 120 mg/kg, single dose) and Nitrosomorpholine (NMOR, 50 ppm, 21 weeks orally) were used to induce HCC in rats. At the end of the experiment, the animals were euthanized under appropriate conditions and samples were collected for biochemical and pathological investigations. In the PC group, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transpeptidase (GGT) levels were higher (p < 0.001) and urea levels were lower (p < 0.001) compared to all other groups. Treatment groups reorganized the relevant markers (ALT, AST, GGT, and urea). A significant increase was detected in Caspase-10, Caspase-3 and Granzyme-B (GrzB) (p < 0.001) in blood and Caspase-10 and GrzB (p < 0.05) in liver tissue in PCT, PCS and PCTS groups compared to the PC group. Histopathological examination revealed that the PC group showed cancer morphology, and the treatment groups caused a decrease in tumor incidence and size. Our current findings suggest that the mechanism of action of TCAE in HCC is through the NKs/CTLs-GrzB-Casp10-Casp3 signaling pathway and can be used in combination with chemotherapy drugs for the development of future drug designs.

El cáncer colorrectal (CCR) se define como el cáncer de colon y recto, y se encuentra entre las principales causas de mortalidad en los países desarrollados. Se informa que el extracto alcohólico de Tarántula cubensis (TCAE) y el destilado de Nerium oleander (NOD) tienen actividad anticancerígena y antioxidante. En este estudio, el objetivo fue investigar los efectos de TCAE y NOD administrados simultáneamente sobre los marcadores de proliferación celular en el cáncer de colon experimental. En el estudio se utilizaron un total de 24 ratas, 6 en cada grupo. Control del Cáncer (CC). se administró azoximetano al comienzo del experimento a una dosis de 15 miligramos (mg)·kilogramos^-1 (kg) (subcutánea, SC) dos veces, con una semana (sem) de diferencia, para inducir el cáncer. CC+TCAE: la dosis de Azoximetano administrada fue de 15 mg·kg^-1 (SC) dos veces por sem al inicio del experimento, mientras que en el caso de TCAE fue de 0,2 mL·kg^-1 (SC) una vez por sem durante 18 sem desde el inicio del experimento. Se administraron 15 mg·kg^-1 (SC) de azoximetano dos veces a intervalos de una sem al comienzo del experimento al grupo CC+NOD, y se administró destilado de NO (NOD) con agua durante todo el experimento. Posteriormente, los animales fueron sacrificados en condiciones apropiadas, se realizaron bloques de parafina formados a partir de tejidos de colon, AgNOR histoquímico (regiones organizadoras nucleolares teñidas con plata) e inmunohistoquímico PCNA (antígeno nuclear de células proliferantes) se realizaron. En el estudio, inmunohistoquímicamente, las puntuaciones de PCNA y el recuento de AgNOR por núcleo (AgNCI) se redujeron significativamente en los grupos C-TCAE y C-NOD (P<0,001). Las puntuaciones del índice de área AgNOR (AgNAI) (P<0,01), el índice de área central (CAI) (P<0,05) y el índice de área AgNOR/índice de área central (AgNAI/CAI) (P<0,01) se redujeron significativamente en el C-TCAE grupo. Como resultado se concluyó que, tanto TCAE como NOD son efectivos como fármacos quimiopreventivos y que TCAE presenta un efecto antiproliferativo más pronunciado que NOD.