Tetrandrine attenuates SNI-induced mechanical allodynia by inhibiting spinal CKLF1

Zhang, Zhi-Ling; Wang, Zhi-Tong; Shi, Jiandang; Pu, Xiaoping; Zhai, Suodi

doi:10.1016/j.neuropharm.2023.109673

Cited by 6 publications

(3 citation statements)

References 32 publications

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“…Notably, the dosages of TET and pregabalin (45 mg/kg) adhered to the recommended dose based on human/mouse dosage conversion ( Nair et al, 2018 ), as indicated in the instructions. It was observed that while 45 mg/kg of TET did not impair the mice’s mobility or induce drowsiness, pregabalin did cause drowsiness ( Zhang et al, 2023 ). Complementing these findings, our prior research also indicated that TET alleviated NP resulting from nerve damage ( Zhang et al, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

“…It was observed that while 45 mg/kg of TET did not impair the mice’s mobility or induce drowsiness, pregabalin did cause drowsiness ( Zhang et al, 2023 ). Complementing these findings, our prior research also indicated that TET alleviated NP resulting from nerve damage ( Zhang et al, 2023 ). Collectively, these results suggest that TET is a promising candidate for OINP therapy.…”

Section: Discussionmentioning

confidence: 99%

“… Zhao et al (2014) reported that TET alleviates LPS-induced abnormal pain by inhibiting the production of prostaglandin 2 (PGE2) and cyclooxygenase 2 (COX-2) through the IKKβ/IκB/NF-κB pathway ( Qin et al, 2018 ). TET also inhibited mechanical allodynia and interleukin 1β (IL-1β) and tumor necrosis factor alpha (TNF-α) of spared nerve injury induced NP mice ( Zhang et al, 2023 ). However, it is currently unclear whether the anti-inflammatory effects of TET are protective in OINP.…”

Section: Introductionmentioning

confidence: 99%

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Tetrandrine alleviates oxaliplatin-induced mechanical allodynia via modulation of inflammation-related genes

Zhang,

Wu,

Liu

et al. 2024

Front. Mol. Neurosci.

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Oxaliplatin, a platinum-based chemotherapy drug, causes neuropathic pain, yet effective pharmacological treatments are lacking. Previously, we showed that tetrandrine (TET), with anti-inflammatory properties, reduces mechanical allodynia in nerve-injured mice. This study explores the effect of TET on oxaliplatin-induced mechanical allodynia and gene changes in mice. Male C57BL/6J mice received oxaliplatin intraperitoneally to induce mechanical allodynia. Post-treatment with TET or vehicle, the mechanical withdrawal threshold (WMT) was assessed using von Frey filaments. TET alleviated oxaliplatin-induced mechanical allodynia. RNA sequencing identified 365 differentially expressed genes (DEGs) in the Control vs. Oxaliplatin group and 229 DEGs in the Oxaliplatin vs. TET group. Pearson correlation analysis of co-regulated DEGs and inflammation-related genes (IRGs) revealed 104 co-regulated inflammation-related genes (Co-IRGs) (|cor| > 0.8, P < 0.01). The top 30 genes in the PPI network were identified. Arg2, Cxcl12, H2-Q6, Kdr, and Nfkbia were highlighted based on ROC analysis. Subsequently, Arg2, Cxcl12, Kdr, and Nfkbia were further verified by qRCR. Immune infiltration analysis indicated increased follicular CD4 T cell infiltration in oxaliplatin-treated mice, reduced by TET. Molecular docking showed strong binding affinity between TET and proteins encoded by Arg2, Cxcl12, Kdr, and Nfkbia. In summary, TET may alleviate oxaliplatin-induced peripheral neuropathy in clinical conditions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%