Mangiferin attenuates contusive spinal cord injury in rats through the regulation of oxidative stress, inflammation and the Bcl-2 and Bax pathway

Abstract

Mangiferin has antioxidant, antiviral, apoptosis regulating, anti‑inflammatory, antitumor and antidiabetic effects, which can also inhibit osteoclast formation and bone resorption. However, whether mangiferin ameliorates the neurological pain of spinal cord injury (SCI) in ratS remains to be elucidated. The present study investigated the therapeutic effects of mangiferin on neurological function, the water content of spinal cord, oxidative stress, the expression of inflammatory cytokines and the protein expression of Bcl‑2/Bax in a SCI rat model. In the present study, the Basso, Beattie and Bresnahan scores, and the water content of the spinal cord were used to analyze the therapeutic effects of mangiferin on neurological pain in the SCI rat. The concentrations of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and the serum levels of glutathione peroxidase (GSH‑PX), nuclear factor‑κB p65 unit, tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and caspase‑3/9 were detected using commercial kits. The expression levels of Bcl‑2 and Bax were measured using western blot analysis. The results demonstrated that administrating mangiferin began to ameliorate neurological function and the water content of the spinal cord in the SCI rat. The mangiferin‑treated group were found to have lower oxidative stress activity and lower expression levels of inflammatory cytokines, compared with the SCI rat. In addition, mangiferin significantly reduced the protein expression of Bax and promoted the protein expression of Bcl-2 in the SCI rat model. Finally, mangiferin markedly suppressed the expression of caspase‑3/9, indicating that the protective action of mangiferin may be associated with anti‑apoptosis activation. In conclusion, mangiferin attenuated contusive SCI in the rats through regulating oxidative stress, inflammation and the Bcl‑2 and Bax pathway.

Mangiferin: A xanthonoid with multipotent anti‐inflammatory potential

“…Interestingly, mangiferin ameliorates not only brain injury but also spinal cord injuries. In neurological pain due to contusive spinal cord injury in rats, mangiferin amended the water content of the spinal cord, the expression levels of inflammatory cytokines and apoptosis‐related proteins, thus attenuating contusive spinal cord injury in rats .…”

Glucagon‐like peptide 2 decreases osteoclasts by stimulating apoptosis dependent on nitric oxide synthase

“…Furthermore, a report indicates that protocatechuic acid prevents osteoclast differentiation through regulating oxidative stress, inflammation and inducing apoptosis in RAW264.7 murine macrophage cells . In particular, avenanthramides (AVAs) with antioxidant properties increase osteoclast apoptosis and mangiferin can also inhibit osteoclast formation and bone resorption through regulating oxidative stress, inflammation and the Bcl‐2 and Bax pathway …”

“…37 In particular, avenanthramides (AVAs) with antioxidant properties increase osteoclast apoptosis 38 and mangiferin can also inhibit osteoclast formation and bone resorption through regulating oxidative stress, inflammation and the Bcl-2 and Bax pathway. 39 In addition, IL-15 stimulates apoptosis of osteoblasts via activation of NK cells by Caspase3. 40 Strikingly, in the report, we first proved that GLP2 exerts its effect in part through the upregulation of iNOS expression.…”

Therapeutic Effect of Curcumin and Methylprednisolone in the Rat Spinal Cord Injury

“…Both Bax and Bcl‐2 are quintessential genes in the Bcl‐2 family and represent apoptotic as well as anti‐apoptotic genes, respectively. The ratio of Bcl‐2 to Bax is considered a decisive factor and plays an important role in determining whether or not cells will undergo apoptosis (Mohammadi et al, ; Luo et al, ). Our results indicated that Bax positive cells gradually abated and was subsequently chaperoned by the upregulation of intensity in the anterior horn of the spinal cord in both Cur‐ and MP‐treated groups.…”