Irradiation adversely affects the repair and regeneration of wounds causing negative impact on the clinical outcome. Therefore, it is necessary to screen newer paradigms that may help to mitigate the deleterious effects of ionizing radiations. Hesperidin (hesperitin-7-rhamnoglucoside or hesperitin-7-rutinoside), a predominant bioflavonoid found in citrus fruits has been evaluated for its wound healing activity in mice whole-body exposed to 2,4, 6 or 8 Gy of γ-radiation. A full-thickness skin wound was created on the dorsum of mice after exposure to various doses of γ-radiation and the wound repair and regeneration was assessed by capturing video images of the excision wounds periodically as a measure of wound contraction as well as by assessing the mean wound healing time. In addition, the biochemical profiles including collagen, hexosamine, DNA, and nitric oxide syntheses were estimated in the granulation tissues at various days postirradiation after exposure to 0 or 6 Gy. In a separate experiment histological information on fibroblast and blood vessel densities were collected in the regenerating granulation tissue at various post-irradiation days after 0 or 6 Gy irradiation. The whole-body exposure of mice to different doses of γ-radiation resulted in a dose dependent delay in the wound contraction and prolongation of wound healing time, where the highest delay was observed after 8 Gy irradiation. Administration of hesperidin orally before irradiation significantly reduced the radiation-induced delay in the wound contraction and mean wound healing time. The collagen, hexosamine, DNA and nitric oxide syntheses were significantly reduced after exposure to 6 Gy, whereas pretreatment with hesperidin significantly enhanced synthesis of collagen, hexosamine, DNA, and nitric oxide. Histological examination revealed an increased rise in fibroblast and vascular densities after treatment with hesperidin in comparison with 6 Gy irradiation. The study demonstrates that hesperidin treatment accelerated the healing of irradiated wounds by increasing the collagen, hexosamine, DNA, and nitric oxide syntheses and increasing the densities of fibroblasts and blood vessels in the

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Ionizing radiations are in frequent clinical use to treat cancer either alone or in combination with surgery or chemotherapy. The radioresistance of tumors is a stumbling block to realize the full potential of radiotherapy. Therefore, pharmacophores that reduce the radioresistance of tumors may be of great importance during tumor therapy. In the present study an attempt has been made to evaluate the potential of dichloromethane extract of giloe i.e. Tinospora cordifolia (TCE) in cultured HeLa cells. Exposure of HeLa cells to TCE for 4 h before exposure to 2 Gy γ-radiation led to a significant decrease in the cell viability (approximately 50 %) accompanied by a reduction in the surviving fraction (SF) up to 0.52 after 4 h of TCE treatment. Thereafter, clonogenecity of HeLa cells declined negligibly with increase in treatment duration up to 6 h post-treatment. There has been a dose dependent attrition in the cell viability of HeLa cells exposed to 1-4 Gy γ-irradiation, whereas treatment of HeLa cells with various doses of TCE further decreased the cell viability depending not only on the irradiation dose but also on the concentration of TCE. The irradiation of HeLa cells resulted in a radiation dose dependent decline in the SF and increasing TCE concentration before irradiation caused a further TCE concentration dependent reduction in SF, and a lowest SF was observed for 4 µg/ml TCE for all irradiation doses. Treatment of HeLa cells with different concentrations of TCE before 3 Gy irradiation resulted in a concentration dependent depletion in glutathione-S-transferase activity until 12 h post-irradiation, whereas lactate dehydrogenase and lipid peroxidation increased up to 4 h post-irradiation and declined gradually thereafter up to 12 h post-irradiation. The TCE treatment increased the radiosensitivity of HeLa cells by reducing glutathione-S-transferase activity and increasing the activity of lactate dehydrogenase and lipid peroxidation.