scholarly journals TNF-ɑ Induces Methylglyoxal Accumulation in Lumbar Herniated Disc of Patients With Radicular Pain

2021 ◽  
Vol 15 ◽  
Author(s):  
Xinsheng Zhang ◽  
Xiaogang Wang ◽  
Liang Gao ◽  
Bin Yang ◽  
Yahan Wang ◽  
...  
Keyword(s):  
Lumbar Disc ◽  
Radicular Pain ◽  
Spinal Nerve ◽  
Herniated Disc ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Underlying Mechanisms ◽  
Rate Limiting ◽  
Activity Decrease ◽  
Necrosis Factor

Lumbar disc herniation (LDH) with radicular pain is a common and complicated musculoskeletal disorder. Our previous study showed that LDH-induced methylglyoxal (MG) accumulation contributed to radicular pain. The underlying mechanisms through which MG accumulates are poorly understood. In the present study, we found that both MG and tumor necrosis factor-alpha (TNF-ɑ) levels in the herniated disc of patients with radicular pain were significantly increased, and the activity of Glyoxalase 1 (GLO1), the rate-limiting enzyme that metabolizes MG, was decreased. In rats, the LDH model was mimicked by implantation of autologous nucleus pulposus (NP) to the left lumbar five spinal nerve root. The mechanical allodynia was observed in LDH rats. Besides, MG and TNF-ɑ levels were increased, and GLO1 activity was significantly decreased in the implanted NP. In cultured rat NP cells, stimulation with the inflammatory mediator TNF-ɑ reduced GLO1 activity and expression. These results suggested that TNF-ɑ-induced GLO1 activity decrease contributed to MG accumulation in the herniated disc of patients with radicular pain.

scholarly journals Tumor Necrosis Factor-alpha and Apoptosis Following Spinal Nerve Ligation Injury in Rats

2011 ◽  
Vol 24 (4) ◽  
pp. 185 ◽  
Author(s):  
Sung Hoon Kim ◽  
Jae Sik Nam ◽  
Dae Kee Choi ◽  
Won Wook Koh ◽  
Jeong Hun Suh ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Spinal Nerve ◽  
Spinal Nerve Ligation ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Modulatory effects of perindopril on cisplatin-induced nephrotoxicity in mice: Implication of inflammatory cytokines and caspase-3 mediated apoptosis

2020 ◽  
Vol 70 (4) ◽  
pp. 515-525 ◽  
Author(s):  
Naif Aljuhani ◽  
Raed S. Ismail ◽  
Mohammed S. El-Awady ◽  
Memy H. Hassan
Keyword(s):  
Caspase 3 ◽  
Weight Ratio ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
Once Daily ◽  
Renal Histology ◽  
Protein Expressions ◽  
Factor Alpha ◽  
Underlying Mechanisms ◽  
Necrosis Factor

AbstractCisplatin-induced nephrotoxicity limits its anticancer effectiveness, thus this study’s aim was to assess the potential modulatory effect of perindopril on cisplatin-induced nephrotoxicity and to elucidate the possible underlying mechanisms. Renal dysfunction was induced in mice by a single injection of cisplatin (10 mg kg−1, i.p.) and perindopril was administered orally (2 mg kg−1, once daily) for 5 days. Perindopril remarkably ameliorated cisplatin-induced perturbations in renal histology, renal levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-10, apoptosis-regulating protein expressions (Bax and Bcl2), and partially normalized Bax to Bcl2 ratio and active caspase 3 protein expression. Conversely, perindopril had no significant effect on cisplatin-induced elevations in serum creatinine and urea, microalbuminuria, kidney to body weight ratio, lipid peroxidation marker, superoxide dismutase and catalase activities and reduced glutathione content. In conclusion, perindopril may be safely used with cisplatin in mice since it ameliorated cisplatin-induced histopathological changes, inflammation and apoptosis without affecting renal biomarkers or oxidative stress.

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