GENOPROTECTIVE EFFECTS OF ETHANOLIC STEM EXTRACTS OF TINOSPORA CORDIFOLIA ON SODIUM ARSENITE-INDUCED DNA DAMAGE IN SWISS MICE LYMPHOCYTES BY COMET ASSAY

Objective: The study was aimed to evaluate the DNA protective effects of ethanolic extracts of Tinospora cordifolia stem on Swiss albino mice lymphocytes against the sodium arsenite-induced genotoxicity. Methods: In this experiment, 25 animals of nearly the same age were equally divided. Group 1 (control) fed on tap water while rest four (2, 3, 4, and 5) groups were treated with 4 mg/kg body weight, per orally sodium arsenite for 12 weeks. Sodium arsenite pretreated groups (4 and 5) were followed by administration of 80 mg/kg body weight, per orally T. cordifolia extracts for the next 12 weeks. Animals were sacrificed at the 8th week and 12th week, respectively, for the assessment of sodium arsenite-induced genotoxicity and comparative genoprotective effects of experimental plant extracts. The extent of DNA migration is directly proportional to the magnitude of DNA damage. Percentage tail DNA content and olive tail moment parameters were used in the comet to relate DNA damage. Results: The findings suggested that the ethanolic stem extracts of T. cordifolia significantly inhibited the sodium arsenite-induced oxidative genotoxicity. The phytoconstituents of T. cordifolia shown to retard genetic damage associated with arsenic exposure. Conclusion: T. cordifolia may be used as a preventive herbal preparation against chemical or arsenical toxicity

EVALUATION OF ANTICLASTOGENIC POTENTIAL OF CINNAMOMUM CASSIA BARK EXTRACT AGAINST ARSENIC GENOTOXICITY BY USING MICRONUCLEUS ASSAY IN MUS MUSCULUS CAUDAL ERYTHROCYTES

Objective: The study was aimed to evaluate the anticlastogenic potential of ethanolic extract of Cinnamomum cassia against arsenic-induced genotoxicity.Methods: In the experiment, 30 animals were taken and divided into five groups and each group contains six animals. Group 1 was control and fed on tap water of Patna city while rest four (2, 3, 4, 5) groups were treated with 4 mg/kg body weight, per orally sodium arsenite for 8 weeks. Sodium arsenite pre-treated Groups 4 and 5 were followed by dose of 100 mg/kg body weight of 5% ethanolic solution of test plant bark extract for next 8 weeks (total duration of dosing 16 weeks). Caudal blood collected from each mouse by minor nick without their sacrifice and smeared blood was stained by double staining. Approximately, 2000 cells were scored by light microscopy to determine micronucleus (MN) frequency. The percentage of MN frequency was expressed in the terms of mean and standard deviation.Results: High index of MN frequency was observed in the Groups 2 and 3 while its frequency drastically reduced in Groups 4 and 5. The mean number of MN scored per 2000 cell were found to be 4.5, 23.5, 18.8, 10.5, and 9.66 in animal Groups 1, 2, 3, 4, 5,respectively.Conclusion: C. cassia may be effective drug in the area of preventive cancer or other kinds of diseases which lead to damage of genetic materials

Amputation-induced reactive oxygen species are required for successful Xenopus tadpole tail regeneration.

Understanding the molecular mechanisms that promote successful tissue regeneration is critical for continued advancements in regenerative medicine. Vertebrate amphibian tadpoles of the species Xenopus laevis and Xenopus tropicalis have remarkable abilities to regenerate their tails following amputation, through the coordinated activity of numerous growth factor signalling pathways, including the Wnt, Fgf, Bmp, Notch and TGF-β pathways. Little is known, however, about the events that act upstream of these signalling pathways following injury. Here, we show that Xenopus tadpole tail amputation induces a sustained production of reactive oxygen species (ROS) during tail regeneration. Lowering ROS levels, using pharmacological or genetic approaches, reduces the level of cell proliferation and impairs tail regeneration. Genetic rescue experiments restored both ROS production and the initiation of the regenerative response. Sustained increased ROS levels are required for Wnt/β-catenin signalling and the activation of one of its main downstream targets, fgf20 (ref. 7), which, in turn, is essential for proper tail regeneration. These findings demonstrate that injury-induced ROS production is an important regulator of tissue regeneration

Immunotherapy for Alzheimer's Disease: Current Scenario and Future Perspectives.

Alzheimer's disease (AD) is a global health concern owing to its complexity, which often poses a great challenge to the development of therapeutic approaches. No single theory has yet accounted for the various risk factors leading to the pathological and clinical manifestations of dementia-type AD. Therefore, treatment options targeting various molecules involved in the pathogenesis of the disease have been unsuccessful. However, the exploration of various immunotherapeutic avenues revitalizes hope after decades of disappointment. The hallmark of a good immunotherapeutic candidate is not only to remove amyloid plaques but also to slow cognitive decline. In line with this, both active and passive immunotherapy have shown success and limitations. Recent approval of aducanumab for the treatment of AD demonstrates how close passive immunotherapy is to being successful. However, several major bottlenecks still need to be resolved. This review outlines recent successes and challenges in the pursuit of an AD vaccine

Mechanisms for suppressing NADPH oxidase in the vascular wall

Oxidative stress underlies many forms of vascular disease as well as tissue injury following ischemia and reperfusion. The major source of oxidative stress in the artery wall is an NADPH oxidase. This enzyme complex as expressed in vascular cells differs from that in phagocytic leucocytes both in biochemical structure and functions. The crucial flavin-containing catalytic subunits, Nox1 and Nox4, are not found in leucocytes, but are highly expressed in vascular cells and upregulated with vascular remodeling, such as that found in hypertension and atherosclerosis. The difference in catalytic subunits offers the opportunity to develop "vascular specific" NADPH oxidase inhibitors that do not compromise the essential physiological signaling and phagocytic functions carried out by reactive oxygen and nitrogen species. Nitric oxide and targeted inhibitors of NADPH oxidase that block the source of oxidative stress in the vasculature are more likely to prevent the deterioration of vascular function that leads to stroke and heart attack, than are conventional antioxidants. The roles of Nox isoforms in other inflammatory conditions are yet to be explored