Polaprezinc reduces paclitaxel-induced peripheral neuropathy in rats without affecting anti-tumor activity

Tsutsumi, Kuniaki; Kaname, Takanori; Shiraishi, Haruka; Kawashiri, Takehiro; Egashira, Nobuaki

doi:10.1016/j.jphs.2016.04.019

Cited by 17 publications

(12 citation statements)

References 12 publications

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“…After activation, NF-κB regulates the expression of genes such as those encoding the inflammatory cytokines TNF-α, IL-1, and IL-6 that can directly or indirectly affect microvascular endothelial cells or blood cells to mediate their interaction, which leads to the dysfunction of microcirculation, endothelial cell, and tissue injury. 18…”

Section: Resultsmentioning

confidence: 99%

“…After activation, NF-jB regulates the expression of genes such as those encoding the inflammatory cytokines TNF-a, IL-1, and IL-6 that can directly or indirectly affect microvascular endothelial cells or blood cells to mediate their interaction, which leads to the dysfunction of microcirculation, endothelial cell, and tissue injury. 18 Ohata et al, 19 found that PZ protects against lipopolysaccharide-induced endotoxin shock via inhibition of NF-jB activation and subsequent induction of proinflammatory products including NO and TNF-a. In the present study, we show that the levels of NF-jB in the brain increased significantly after rats were administered CTX or DDP alone.…”

Section: Effects Of Px Combined With Ctx or Ddp On The Gastric Mucosamentioning

confidence: 99%

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Effects of polaprezinc on gastric mucosal damage and neurotransmitters in a rat model of chemotherapy-induced vomiting

Liu

Xie

et al. 2018

J Int Med Res

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ObjectiveTo investigate the effects of polaprezinc (PZ) on cyclophosphamide (CTX)- or cisplatin (DDP)-induced gastric mucosal injury and on a rat model of neurotransmitter-mediated vomiting.MethodsSprague–Dawley rats were divided at random into Control, CTX, DDP, PZ+CTX, and PZ+DDP groups. After 20 days, brain tissues and sera were analyzed for the levels of dopamine (DA), 5-hydroxytryptamine (5-HT), and nuclear factor kappa B (NF-κB). Hematoxylin and eosin-stained sections of stomach, intestine, and brain tissues were examined using light microscopy.ResultsThe levels of DA, 5-HT, and NF-κB in brain and serum samples of rats treated with CTX or DDP were significantly increased compared with those of rats in the Control group. There was a significant decrease in these values in the PZ group. Moreover, PZ reduced damage to brain tissue caused by CTX or DDP.ConclusionsPZ decreased the levels of DA, 5-HT, and NF-κB in blood and brain tissues caused by CTX or DDP and reduced the chemotherapy-induced damage to the small intestine, stomach, and brain. These findings can be translated to the clinic to enhance the efficacy and safety of chemotherapy.

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Section: Resultsmentioning

confidence: 99%

Section: Effects Of Px Combined With Ctx or Ddp On The Gastric Mucosamentioning

confidence: 99%

Effects of polaprezinc on gastric mucosal damage and neurotransmitters in a rat model of chemotherapy-induced vomiting

Liu

Xie

et al. 2018

J Int Med Res

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“…Induction of neuropathic pain and dosing PTX (4 mg/kg) was injected intraperitoneally (i.p.) in volumes of one ml per kg, four times a week (on days 1, 3, 5, and 7) [32]. PTX dose selection was presumed on a previous report [32].…”

Section: Methodsmentioning

confidence: 99%

“…in volumes of one ml per kg, four times a week (on days 1, 3, 5, and 7) [32]. PTX dose selection was presumed on a previous report [32]. 1 was administered once daily for 8 days (5 and 10 mg).…”

Section: Methodsmentioning

confidence: 99%

Anti-Neuropathic Pain Activity of A Cationic Palladium (II) Dithiocarbamate By Suppressing The Inflammatory Mediators in Paclitaxel-Induced Neuropathic Pain Model

Naveed

Ullah

Khan

et al. 2021

Preprint

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Neuropathic pain is an obstinate chronic pain state which extremely worsens the quality of life of the suffered population. It is still intended as an intractable disease as existing therapies are not excellent in terms of efficacy and tolerability. Therefore, to search for novel drugs are crucial to acquire satisfactory treatments. The present study investigated the possible antiallodynic, antihyperalgesic and neuroprotective activities of (1,4-bis-(diphenylphosphino) butane) palladium (II)chloride monohydrate-(1) in Paclitaxel (PTX)-induced neuropathic pain model (Fig.10). Initially, 1 (5 and 10 mg/kg, b.w) was investigated for antinociceptive activities at behavioral level by performing mechanical and cold allodynia as well as thermal and tail immersion hyperalgesia. RT-PCR was performed to determine the suppressing effect of 1 on mRNA expression level of iNOS, COX-2 and proinflammatory cytokines (TNF-α, IL-1β, IL-6). In addition, antioxidant protein and enzymes (GSH, GST, Catalase), NO, MDA level and muscle activity were also determined. The results demonstrate that once daily dosing of 1 significantly repressed the behavioral pain responses dose dependently. Moreover, the mRNA gene expression of iNOS, COX-2 and inflammatory cytokines were reduced noticeably by 1. Furthermore, the treatment enhanced the level of antioxidant enzymes and lowered the level of MDA and NO production with no effect on motor activities of rats. These findings suggest the potential of 1 to attenuate neuropathic pain, neuroinflammation and neuroprotective effect. Thereupon, 1 might be a dynamic candidate for the therapeutic management of chronic neuropathic pain.

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“…Inflammatory cytokines (e.g., interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)) and chemokines (e.g., chemokine (C-X-C motif) ligand (CXCL) family) were elevated in the peripheral sites, spinal cord, and of paclitaxeltreated animals, and many agents reduced the peripheral neuropathy symptoms via their anti-inflammatory effects [19,21,22,24,25,27,28,[32][33][34][35][36][37][38][39]41,42,[44][45][46][47][49][50][51][52][53][54]56]. Activations of astrocytes and microglia were also observed in the spinal dorsal horn after paclitaxel administrations, and many agents including minocycline attenuated PIPN via the inhibition of these spinal changes and prevented neurological damage [40,43,44,48].…”

Section: Anti-inflammatory Agentsmentioning

confidence: 99%

Preclinical and Clinical Evidence of Therapeutic Agents for Paclitaxel-Induced Peripheral Neuropathy

Kawashiri

Inoue

Mori

et al. 2021

IJMS

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Paclitaxel is an essential drug in the chemotherapy of ovarian, non-small cell lung, breast, gastric, endometrial, and pancreatic cancers. However, it frequently causes peripheral neuropathy as a dose-limiting factor. Animal models of paclitaxel-induced peripheral neuropathy (PIPN) have been established. The mechanisms of PIPN development have been elucidated, and many drugs and agents have been proven to have neuroprotective effects in basic studies. In addition, some of these drugs have been validated in clinical studies for their inhibitory PIPN effects. This review summarizes the basic and clinical evidence for therapeutic or prophylactic effects for PIPN. In pre-clinical research, many reports exist of neuropathy inhibitors that target oxidative stress, inflammatory response, ion channels, transient receptor potential (TRP) channels, cannabinoid receptors, and the monoamine nervous system. Alternatively, very few drugs have demonstrated PIPN efficacy in clinical trials. Thus, enhancing translational research to translate pre-clinical research into clinical research is important.

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Polaprezinc reduces paclitaxel-induced peripheral neuropathy in rats without affecting anti-tumor activity

Cited by 17 publications

References 12 publications

Effects of polaprezinc on gastric mucosal damage and neurotransmitters in a rat model of chemotherapy-induced vomiting

Effects of polaprezinc on gastric mucosal damage and neurotransmitters in a rat model of chemotherapy-induced vomiting

Anti-Neuropathic Pain Activity of A Cationic Palladium (II) Dithiocarbamate By Suppressing The Inflammatory Mediators in Paclitaxel-Induced Neuropathic Pain Model

Preclinical and Clinical Evidence of Therapeutic Agents for Paclitaxel-Induced Peripheral Neuropathy

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