METHOD: Cleistanthins A and B were isolated from the leaves of Cleistanthus collinus. Both the compounds were administered orally for 90 days at the concentration of 12.5, 25 and 50 mg/kg, and the effects on blood pressure, biochemical parameters and histology were assessed. The dose for sub-chronic toxicology was determined by fixed dose method according to OECD guidelines.
RESULT: Sub-chronic toxicity study of cleistanthins A and B spanning over 90 days at the dose levels of 12.5, 25 and 50 mg/kg (once daily, per oral) revealed a significant dose dependant toxic effect in lungs. The compounds did not have any effect on the growth of the rats. The food and water intake of the animals were also not affected by both cleistanthins A and B. Both the compounds did not have any significant effect on liver and renal markers. The histopathological analysis of both cleistanthins A and B showed dose dependent morphological changes in the brain, heart, lung, liver and kidney. When compared to cleistanthin A, cleistanthin B had more toxic effect in Wistar rats. Both the compounds have produced a dose dependent increase of corpora amylacea in brain and induced acute tubular necrosis in kidneys. In addition, cleistanthin B caused spotty necrosis of liver in higher doses.
CONCLUSION: The present study concludes that both cleistanthin A and cleistanthin B exert severe toxic effects on lungs, brain, liver, heart and kidneys. They do not cause any significant pathological change in the reproductive system; neither do they induce neurodegenerative changes in brain. When compared to cleistanthin A, cleistanthin B is more toxic in rats.
Materials and Methods: Three months old Sprague Dawley male rats were randomly divided into 5 groups: (I) control group; (II) alcohol (3g/kg) + normal saline; (III) alcohol (3g/kg) + olive oil; (IV) alcohol (3g/kg) + alpha-tocopherol (60mg/kg) and (V) alcohol (3g/kg) + palm vitamin E (60mg/kg). The treatment lasted for three months. Following sacrifice, the right tibia was subjected to bone biomechanical test while the lumbar (fourth and fifth lumbar) and left tibia bones were harvested for bone mineral measurement.
Results: Alcohol caused reduction in bone biomechanical parameters (maximum force, ultimate stress, yield stress and Young's modulus) and bone minerals (bone calcium and magnesium) compared to control group (P<0.05). Palm vitamin E was able to improve bone biomechanical parameters by increasing the maximum force, ultimate stress and Young's modulus (P<0.05) while alpha-tocopherol was not able to. Both alpha-tocopherol and palm vitamin E were able to significantly increase tibia calcium and magnesium content while only alpha-tocopherol caused significant increase in lumbar calcium content (P<0.05).
Conclusion: Both palm vitamin E and alpha-tocopherol improved bone mineral content which was reduced by alcohol. However, only palm vitamin E was able to improve bone strength in alcohol treated rats.
Materials and Methods: Twenty-four: Sprague Dawley rats were equally distributed into the following four groups: G1 (control), G2, G3, and G4 represented the groups treated with EBN at graded concentrations of 0, 30, 60, and 120 mg/kg body weight (BW) per day for 8 weeks, respectively. During the experimental period, the BW of each rat was recorded weekly. At the proestrus stage of estrous cycle, blood samples were collected from the hearts of anesthetized rats that were later sacrificed. The uteri were removed for histological and immunohistochemical analyses.
Results: The EBN-treated groups showed an increase in the weights and lengths of uteri as compared to the control. Results showed that relative to G1 and G2, G3 and G4 exhibited proliferation in their uterine luminal and glandular epithelia and uterine glands, and up-regulated expressions of EGF, REGF, VEGF, PCNA, and progesterone receptor, and estrogen receptor in their uteri. The EBN increased the antioxidant (AO) and total AO capacities and reduced the oxidative stress (OS) levels in non-pregnant rats.
Conclusion: Findings of this study revealed that EBN promotes proliferation of the uterine structures as evidenced by the upregulation of the expressions of steroid receptors, EGF, REGF, VEGF, and PCNA in the uterus and increased in the plasma concentrations of AO and reduced levels of OS.
METHODS: Twelve rats were used in the study and divided in to two equal groups. All the animals in the control group were intragastically gavaged by distilled water and continues for ten days, from day 24 to day 34 of age, while the animals in the study group were intragastically gavaged by GT extract (300mg/kg/day) which continues also for ten days from day 24 to day 34 of age. On day 34 of age, and two hours after the last dose, the rats were anaesthetized and blood collection by cardiac puncture was taken.
RESULTS: The results showed that the intragastric gavage of a high dose of GT extract caused a non-significant increase in serum magnesium, and calcium levels (p>0.05), but a significant increase in zinc serum level was seen(p< 0.05).
CONCLUSION: GT can cause a significant increase in zinc serum level, and this may explain the significant role of GT in the response to different oxidative stress. It is recommended to measure the Zn serum level in rats after a period longer than two hrs from the time of the last dose of intragastric gavage of GT extract.