Evaluation of the rivastigmine role against botulinum toxin-A-induced osteoporosis in albino rats: A biochemical, histological, and immunohistochemical study.
D M AliWalaa Yehia AbdelzaherSmn Abdel-HafezPublished in: Human & experimental toxicology (2018)
The present study aimed to evaluate the role of rivastigmine against the effect of a single unilateral botulinum toxin-A (BTX-A) injection on the bone and bone marrow of adult albino rats 4 weeks after injection. Twenty-four Wistar albino rats were divided into four equal groups: group I, which received distilled water; group II, which received rivastigmine (0.3 mg/kg daily, intraperitoneally for 4 weeks); group III, which received BTX-A (4 IU in 0.2 mL physiological saline) single dose, intramuscularly; and group IV, which received BTX-A + rivastigmine. The results revealed that BTX-A induced a significant decrease in the calcium level with a significant increase in the phosphorus, alkaline phosphatase, C-reactive protein, and tumor necrosis factor α levels in serum. Furthermore, a significant increase in malondialdehyde with a significant decrease in reduced glutathione activities in both bone and bone marrow. Histologically, a distortion and thinning out of the compact bone and trabeculae of cancellous bone of the rat femur in the BTX-A group with an increase in adipocytes in adjacent bone marrow were detected. Immunohistochemically, Cluster of Differentiation 68 (CD68) showed a significant increase in both osteoclasts and bone marrow macrophage. Rivastigmine treatment could relieve the toxic effects induced by BTX-A. In conclusion, rivastigmine has a protective effect against the hazardous effects of BTX-A on bone and bone marrow.
Keyphrases
- bone marrow
- bone mineral density
- botulinum toxin
- mesenchymal stem cells
- postmenopausal women
- bone loss
- soft tissue
- bone regeneration
- adipose tissue
- high glucose
- rheumatoid arthritis
- physical activity
- oxidative stress
- type diabetes
- drug induced
- skeletal muscle
- risk assessment
- heavy metals
- insulin resistance
- anaerobic digestion