Methods: Thirty female Sprague-Dawley rats were sorted into 5 groups (n = 6) namely: MPv (leaf treatment); MPr (root treatment); ERT (estrogen treatment); OVXC (untreated ovariectomized control) and Sham (untreated sham-operated control). All rats (except the Sham) were ovariectomized to induce a state of estrogen deficiency that simulates menopause. Two weeks after ovariectomy, the rats were treated for 8 weeks with oral gavages of estrogen and plant extracts. The ERT group received 64.5 μg/kg/day dose of estrogen while MPv and MPr groups received 20 mg/kg/day dose of leaf and root extracts, respectively. At the end of treatment, left femora were excised from euthanized rats and investigated for changes in bone micro-architecture, mineral density, and biomechanical properties.

METHODS: Swiss albino mice (25-30 g) and Wistar rats (150-180 g) under standard controlled conditions (24 ± 2°C, 50-70 humidity and 12 h light/dark cycle). The groups were divided into 6 groups (n = 6/group) and assigned as control, negative control, standard and, formaldehyde supplemented with two different test dose groups of A. aspera for 4 weeks. Arthritis induced by subplantar administration of 0.1 ml formaldehyde (2% v/v) into the left hind paw in all groups except normal control. Arthritis was assessed using serum Hb, ESR, paw volume, joint diameter, radiological and histopathological investigation.

RESULTS: Oral administration of AEAA shown a significant (p < 0.01) dose-dependent protection against formaldehyde induced arthritis. At 21st day, A.asperashown an inhibition of paw volume in the different doses of 250 mg/kg and 500 mg/kg were found to be 30% and, 38.33% respectively. At 14th day the joint swelling was found to be 27.2% and 36.36 respectively. Diclofenac (10 mg/kg) had an effect of 36.61% inhibition of arthritis and joint swelling at 21st and 14th day.

Materials and Methods: Twenty-five ICR mice and 20 BALB/C mice were used where five animals as control and the rest were randomly divided into four time points at 5, 10, 24 and 48 hours post-dosing (hpd). They were induced with 500 mg/kg APAP intraperitoneally. Liver sections were processed for hematoxylin-eosin staining and histopathological changes were scored based on grading methods.

Results: Intense centrilobular damage was observed as early as 5 hpd in BALB/C as compared to ICR mice, which was observed at 10 hpd. The difference of liver injury between ICR and BALB/C mice is due to dissimilarity in the genetic line-up that related to different elimination pathways of APAP toxicity. However, at 24 hpd, the damage was markedly subsided and liver regeneration had taken place for both ICR and BALB/C groups with evidence of mitotic figures. This study showed that normal liver architecture was restored after the clearance of toxic insult.