Clinical significance of SIRT3 and inflammatory factors in multiple myeloma patients with bortezomib-induced peripheral neuropathy: a cohort study

Yang, Huiqi; Liu, Can; Fang, Yuan; Li, Fang

doi:10.1080/00365513.2021.1986857

Cited by 2 publications

(1 citation statement)

References 33 publications

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“…In addition, clinical studies detected significantly higher serum IL6 levels in MM patients after bortezomib treatment than that before the treatment, and patients with elevated IL6 levels present with varying degrees of neuropathy. 16 , 17 This observation suggests that IL6 is an independent risk factor for peripheral neuropathy (PN) in MM patients after bortezomib treatment. 18 Deficiency of Parkin and PINK1 can cause an impairment of mitochondrial autophagy, leading to the release of mitochondrial DNA (mtDNA) and triggering inflammation.…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin Ameliorates BiPN by Reducing IL6 Levels and Regulating PARKIN-Mediated Mitochondrial Autophagy

Sun¹,

Liu²,

Yu³

et al. 2022

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Background Bortezomib-induced peripheral neuropathy (BiPN) is a common complication of multiple myeloma (MM) treatment that seriously affects the quality of life of patients. The purpose of the present study was to explore the therapeutic effect of paeoniflorin on BiPN and its possible mechanism. Methods ELISA was used to measure the level of interleukin-6 (IL6) in the plasma of MM patients, and bioinformatics analysis was used to predict the mechanism underlying the effect of paeoniflorin on peripheral neuropathy. Cell and animal models of BiPN were constructed to evaluate mitochondrial function by measuring cell viability and mitochondrial quality and labeling mitochondria with MitoTracker Green. Nerve injury in mice with BiPN was assessed by behavioral tests, evaluation of motor nerve conduction velocity, hematoxylin-eosin (HE) staining, electron microscopy and analysis of the levels of reactive oxygen species (ROS). Western blotting and immunohistochemistry (IHC) were used to assess the expression of autophagy-related proteins. Results In MM patients, IL6 levels were positively correlated with the degree of PN. The results of bioinformatics analysis suggested that paeoniflorin ameliorated PN by altering inflammation levels and mitochondrial autophagy. Paeoniflorin increased PC12 cell viability and mitochondrial autophagy levels, alleviated mitochondrial damage, and reduced IL6 levels. In addition, paeoniflorin effectively improved the behavior of mice with BiPN, relieved sciatic nerve injury in mice, increased the expression of LC3II/I, beclin-1, and Parkin in sciatic nerve cells, and increased the expression of LC3B and Parkin in the nerve tissue. Conclusion The present study confirmed that paeoniflorin significantly ameliorated peripheral neuropathy (PN) caused by bortezomib, possibly by reducing IL6 levels to regulate PARKIN-mediated mitochondrial autophagy and mitochondrial damage.

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Section: Introductionmentioning

confidence: 99%