The present study was designed to determine the role of topical treatment with curcumin (Cur) on burn wound healing in rats. The Wistar-albino rats were randomly allotted into one of three experimental groups: 4th, 8th and 12th day (post burn) and all groups include subgroups which Burn and Burn + Cur. Each group contains 12 animals. Burn wounds were made on the back of rat and Cur was administered topically. At the end of the study, all animals were sacrificed and the wound tissues removed for analyse to biochemical and histopathological changes. There was a significant increase in the hydroxyproline levels in the skin of the Cur groups. Cur treated wounds were found to heal much faster as indicated by improved rates of inflammatory cells, collagen deposition, angiogenesis, granulation tissue formation and epithelialization which were also confirmed by histopathological and biochemical examinations. Our data also indicate that there is a rise in the expression of proliferating cell nuclear antigen in skin tissues of Cur-treated rats in the Burn group. The results clearly substantiate the beneficial effects of the topical application of Cur in the acceleration of wound healing.
Scrotal hyperthermia has been known as a cause of male infertility but the exact mechanism leading to impaired spermatogenesis is unknown. This work was aimed to investigate the role of scrotal hyperthermia on cell proliferation and apoptosis in testes. The rats were randomly allotted into one of the four experimental groups: A (control), B (1 day after scrotal hyperthermia), C (14 days after scrotal hyperthermia), and D (35 days after scrotal hyperthermia); each group comprised 7 animals. Scrotal hyperthermia was carried out in a thermostatically controlled water bath at 43°C for 30 min once daily for 6 consecutive days. Control rats were treated in the same way, except the testes were immersed in a water bath maintained at 22°C. Hyperthermia-exposed rats were killed under 50 mg/kg ketamine anaesthesia and tissue samples were obtained for biochemical and histopathological investigations. Hyperthermia treatment significantly decreased the testicular antioxidant system, including decreases in the glutathione level, superoxide dismutase, and glutathione peroxidase activities. Moreover, exposure to hyperthermia resulted in lipid peroxidation increase in testes. Our data indicate a significant reduction in the expression of proliferating cell nuclear antigen and an enhancement in the activity of terminal deoxynucleotidyl transferase dUTP nick end labelling after scrotal hyperthermia. In scrotal hyperthermia, the mitochondrial degeneration, dilatation of smooth endoplasmic reticulum, and enlarged intercellular spaces were observed in both Sertoli and spermatid cells. Scrotal hyperthermia is one of the major factors that impair spermatogenesis in testis. This heat stress is shown to be closely associated with oxidative stress, followed by apoptosis of germ cells.
Cadmium (Cd) is one of the environmental pollutants affecting various tissues and organs including testis. The aim of this study was to investigate the anti-apoptotic effects of curcumin (Cur) on Cd-induced apoptosis in rat testes. The rats were randomly allotted into one of three experimental groups: control, Cd treated and Cd treated with Cur; each group contained 10 animals. The control group received 2 ml/day of dimethyl sulfoxide (DMSO). To induce toxicity, Cd (1 mg/kg body weight) was dissolved in normal saline and subcutaneously injected into rats for 4 weeks. The rats in Cur-treated group was given a daily dose of 100 mg/kg of Cur for 4 weeks. To date, no examinations of the anti-apoptotic properties of Cur on Cd-induced apoptosis in rat testes have been reported. The mean seminiferous tubule diameter, mean testicular biopsy score values and serum testosterone levels were significantly decreased in Cd-treated groups were compared to the control group. Furthermore, the Cur-treated animals showed an improved histological appearance and serum testosterone levels in Cd-treated group. Our data indicate a significant reduction in the activity of in situ identification of apoptosis using terminal dUTP nick end-labeling in testis tissues of the Cd-treated group with Cur therapy. The present study showed that Cur treatment protected testes against toxic effects of Cd. We believe that further preclinical research into the utility of Cur may indicate its usefulness as a potential treatment on the spermatogenesis after testicular injury caused by Cd-treated rats.
These results demonstrate that Cur attenuated testicular damage in diabetic rats by decreasing oxidative stress.
The aim of this study was to examine the protective effects of fish omega-3 (n-3) fatty acids on acute doxorubicin (DOX)-induced testicular apoptosis and oxidative damage. 24 male rats were divided into three groups: control, DOX-treated and DOX+fish n-3 fatty acids. Fish n-3 fatty acids (400 mg kg(-1) ) were given for 30 days by intragastric gavage. The rats received a single intraperitoneal injection of DOX (30 mg kg(-1) ) and were sacrificed after 48 h. The DOX+fish n-3 fatty acids group showed a decrease in malondialdehyde levels and increased activities of superoxide dismutase and glutathione peroxidase in comparison with the DOX-treated group. Acute DOX treatment caused severe damage such as disorganisation and separation of germ cells. The fish n-3 fatty acids-pretreated rats showed an improved histological appearance in the DOX-treated group. Our data indicate a reduction in the activity of terminal deoxynucleotidyl transferase mediated dUTP nick end labelling; there was a rise in the expression of proliferating cell nuclear antigen in testis tissues of the DOX+fish n-3 fatty acids group compared with DOX-treated group. These data suggested that fish n-3 fatty acids pre-treatment may be beneficial for spermatogenesis following acute DOX-induced testicular damage by decreasing germ cell apoptosis and oxidative stress.
Cadmium (Cd), an environmental and industrial pollutant, generates free radicals responsible for oxidative stress. Cd can also lead to various renal toxic damage such as the proximal tubules and glomerulus dysfunction. Thymoquinone (TQ) is the main constituent of the essential oil obtained from black seeds (Nigella sativa) and has various pharmacological effects. The aim of the present study was to examine the nephroprotective, anti-oxidant, and anti-apoptotic effect of the TQ against Cd-induced nephrotoxicity. A total of 24 male Wistar albino rats were divided into three groups: control, Cd-treated, and Cd-treated with TQ; each group contain eight animals. The Cd-treated group was injected subcutaneously with CdCl2 dissolved in saline in the amount of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in TQ-treated groups were given TQ (50 mg/kg body weight) once a day orally together with first Cd injection during the study period. The histopathological studies in the kidney of rats also showed that TQ markedly reduced the toxicity of Cd and preserved the normal histological architecture of the renal tissue. Immunohistochemical analysis revealed that TQ significantly decreased the Cd-induced over expression of nuclear factor-κB in renal tissue. Furthermore, TQ treatment resulted in decreased the number of apoptotic cells. TQ significantly suppressed lipid peroxidation, compensated deficits in the anti-oxidant defenses (reduced superoxide dismutase, glutathione peroxidase and catalase activities) in renal tissue resulted from Cd administration. These findings suggest that the nephroprotective potential of TQ in Cd toxicity might be due to its anti-oxidant and anti-apoptotic properties, which could be useful for achieving optimum effects in Cd-induced nephrotoxicity.
We aimed to investigate the preventive effect of Infliximab (IFX), a tumor necrosis factor (TNF)-α inhibitor, on bleomycin (BLC)-induced lung fibrosis in rats. Rats were assigned into four groups as follows: I-BLC group, a single intra-tracheal BLC (2.5 mg/kg) was installed; II-control group, a single intra-tracheal saline was installed; III-IFX + BLC group, a single-dose IFX (7 mg/kg) was administered intraperitoneally (i.p.), 72 h before the intra-tracheal BLC installation; IV-IFX group, IFX (7 mg/kg) was administered alone i.p. on the same day with IFX + BLC group. All animals were sacrificed on the 14th day of BLC installation. Levels of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, interleukin (IL)-6, periostin, YKL-40, nitric oxide (NO) in rat serum were measured, as well as, myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activity, and reduced glutathione (GSH), hydroxyproline, malondialdehyde (MDA) content in lung homogenates. Lung tissues were stained with hematoxylin and eosin (H&E) for quantitative histological evaluation. The inducible nitric oxide synthase (iNOS) expression and cell apoptosis in the lung tissues were determined quantitatively by immunohistochemical staining (INOS) and by TUNNEL staining, respectively. BLC installation worsened antioxidant status (such as SOD, CAT, GPx, GSH, MPO), while it increased the serum TNF-α, TGF-β, IL-6, periostin, YKL-40, and lipid peroxidation, and collagen deposition, measured by MDA and hydroxyproline, respectively. IFX pretreatment improved antioxidant status as well as BLC-induced lung pathological changes, while it decreased the TNF-α, TGF-β, IL-6, periostin, YKL-40, lipid peroxidation and collagen deposition. Finally, histological, immunohistochemical, and TUNNEL evidence also supported the ability of IFX to prevent BLC-induced lung fibrosis. The results of the present study indicate that IFX pretreatment can attenuate BLC-induced pulmonary fibrosis.
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