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 » Introduction
 » Methods
 » Results
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  Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 52  |  Issue : 7  |  Page : 179-181
 

Tashinone II A-sulfoacid-natrum elevates the pain threshold through inhibiting nuclear factor kappa B pathway in neuropathic cancer pain


1 Department of Anesthesiology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, PR China
2 Department of Pharmacy, The People's Hospital of Lishui City, Lishui, Zhejiang, PR China
3 Department of Anesthesiology, The People's Hospital of Lishui City, Lishui, Zhejiang, PR China

Date of Web Publication20-Jul-2016

Correspondence Address:
Z Ling-bin
Department of Anesthesiology, The People's Hospital of Lishui City, Lishui, Zhejiang
PR China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-509X.186575

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 » Abstract 

OBJECTIVE: The purpose of this study was to evaluate the effects of Tashinone II A-sulfoacid-natrum on the pain threshold and potential molecular mechanism for neuropathic cancer pain. METHODS: Forty-five male Balb/c mice were divided into control group model group and experiment group with each 15. The sciatic nerve muscle plexus of experiment and model group were given injection containing S180 sarcoma cell 2 × 10 6 mL for each mouse. Mice in the experiment group were given Tashinone II A-sulfoacid-natrum 25 mg/kg once a day intraperitoneal injection. Moreover, mice in the control group were given physiological saline 25 mg/kg, once a day intraperitoneal injection. The mechanical withdraw threshold and thermal withdraw latency were recorded before S180 sarcoma cell injection and in the time point of day 3, 6, 9, 12, and 14. After 14 days treatment, the mice were treated to death and the sciatic nerve CX3CR1 and nuclear factor kappa B (NF-kB) mRNA was tested by quantitative polymerase chain reaction. RESULTS: Compared with control group, the mechanical and thermal pain threshold of experiment group was significant decreased (P < 0.05). However, compared with the model group, the mechanical, and thermal pain threshold of experiment group was significant elevated in time point of day 3, 6, 9, 12, 14 for mechanical pain threshold and day 9, 12 14 for thermal pain threshold (P < 0.05); the pain threshold for the experiment and model group was decreased in the first 9 days and then elevated gradually. Compared with control group, the CX3CR1 and NF-kB mRNA relative expression in mice sciatic nerve of experiment group was significant elevated (P < 0.05); but compared with model group, the CX3CR1 and NF-kB mRNA relative expression of experiment group was significant decreased (P < 0.05). CONCLUSION: Tashinone II A-sulfoacid-natrum can elevates the mechanical and thermal pain threshold through inhibiting the NF-kB in neuropathic cancer pain rat.


Keywords: Mice, molecular mechanism, neuropathic cancer pain, signal pathway, tashinone II A-sulfoacid-natrum


How to cite this article:
Jian-min T, Jun L, Sheng-yang C, Shuang-mei Y, Shu-e C, Xiu-qin Y, Chen P, Ling-bin Z. Tashinone II A-sulfoacid-natrum elevates the pain threshold through inhibiting nuclear factor kappa B pathway in neuropathic cancer pain. Indian J Cancer 2015;52, Suppl S3:179-81

How to cite this URL:
Jian-min T, Jun L, Sheng-yang C, Shuang-mei Y, Shu-e C, Xiu-qin Y, Chen P, Ling-bin Z. Tashinone II A-sulfoacid-natrum elevates the pain threshold through inhibiting nuclear factor kappa B pathway in neuropathic cancer pain. Indian J Cancer [serial online] 2015 [cited 2018 Dec 13];52, Suppl S3:179-81. Available from: http://www.indianjcancer.com/text.asp?2015/52/7/179/186575



 » Introduction Top


Neuropathic pain is usually caused by damage or disease affecting the somatosensory nervous system which may be associated with abnormal sensations called dysesthesia or pain from normally nonpainful stimuli (allodynia). Neuropathic pain may also result from disorders of the peripheral nervous system or the central nervous system (brain and spinal cord). It was reported that more than 7% of the European population is affected by neuropathic pain, and in 5% of them it may be severe. [1],[2] But the exact mechanism of neuropathic pain was not clear. Some researchers believed that the altered expression of ion channels, changes in neurotransmitters and their receptors as well as altered gene expression in response to neural input is important for the neuropathic pain. [3] Neuropathic pain in cancer arises following injury to peripheral or central neurons, in a similar manner to such pain arising from a noncancer injury. [4]

Recently, report showed that tashinone II A-sulfoacid-natrum can reduced the neuropathic pain in mice. [5] However, its mechanism was not clear. Here, we discuss the effects of tashinone II A-sulfoacid-natrum on the pain threshold and potential molecular mechanism for neuropathic cancer pain.


 » Methods Top


Forty-five male Balb/c mice were divided into control group model group and experiment group with each 15. The sciatic nerve muscle plexus of experiment and model group were given injection containing S180 sarcoma cell 2 × 10 6 mL for each mouse. [6] Mice in the experiment group were given tashinone II A-sulfoacid-natrum 25 mg/kg once a day intraperitoneal injection. Moreover, mice in the control group were given physiological saline 25 mg/kg, once a day intraperitoneal injection. The mechanical withdraw threshold and thermal withdraw latency were recorded before S180 sarcoma cell injection and in the time point of day 3, 6, 9, 12, and 14. After 14 days treatment, the mice were treated to death and the spine cord CX3CR1 and nuclear factor kappa B (NF-kB) mRNA was tested by quantitative polymerase chain reaction.

Statistics

All values are expressed by mean ± standard deviation. The significance of differences was analyzed by an ANOVA test and an unpaired Student's t-test to compare between groups. The data were analyzed using the GraphPad Prism software 5.0 (http://www.graphpad.com/scientific-software/prism/). A significant value was considered at P < 0.05.


 » Results Top


The mechanical pain threshold comparison

Compared with control group, the mechanical pain threshold of experiment group was significant decreased (P < 0.050); but compared with the model group, the mechanical pain threshold of experiment group was significant elevated in time point of day 3, 6, 9, 12, and day 14 (P < 0.05); and the pain threshold for the experiment and model group was decreased in the first 9 days and then elevated gradually, [Figure 1].
Figure 1: The mechanical pain threshold comparison for the three groups

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The thermal pain threshold comparison

Compared with control group, the thermal pain threshold of experiment group was significant decreased (P < 0.05); but compared with the model group, the thermal pain threshold of experiment group was significant elevated in time point of day 9, 12, and day 14 (P < 0.05); and the pain thermal pain threshold for the experiment and model group was decreased in the first 9 days and then elevated gradually, [Figure 2].
Figure 2: The thermal pain threshold comparison for the three groups

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CX3CR1 and nuclear factor kappa B mRNA expression sciatic nerve

Compared with control group, the CX3CR1 and NF-kB mRNA relative expression in mice sciatic nerve of experiment group was significant elevated (P < 0.05); but compared with model group, the CX3CR1 and NF-kB mRNA relative expression of experiment group was significant decreased (P < 0.05), [Figure 3].
Figure 3: CX3CR1 and nuclear factor kappa B mRNA expression sciatic nerve

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 » Discussion Top


Neuropathic pain is defined by the International Association for the Study of Pain as pain that arises as a direct consequence of a lesion or disease affecting the somatosensory system. [7],[8] Neuropathic pain is usually caused by damage or disease affecting the somatosensory nervous system which may be associated with abnormal sensations called dysesthesia or pain from normally nonpainful stimuli (allodynia). [9] It was reported that more than 7% of the European population is affected by neuropathic pain, and in 5% of them it may be severe. [1],[2] However, the exact mechanism of neuropathic pain was not clear. [8],[10],[11] Hence, it is urgent to develop novel mechanism-based therapeutic agents that are highly efficacious and well tolerated to improve relief of neuropathic pain. [12] Neuropathic pain is difficult to treat with only 40-60% of the patients achieving partial relief. [13] Favored treatments are certain antidepressants (tricyclic antidepressant and serotonin-norepinephrine reuptake inhibitors), anticonvulsants (pregabalin and gabapentin), and topical lidocaine. [14] But the efficacy is not satisfaction. Recently, report showed that tashinone II A-sulfoacid-natrum can reduced the neuropathic pain in mice. [5] However, its mechanism was not clear. In our present study, we evaluate the effects of tashinone II A-sulfoacid-natrum on the pain threshold and potential molecular mechanism for neuropathic cancer pain model mice. We find that the mechanical and thermal pain threshold was significant decreased by intraperitoneal injection of tashinone II A-sulfoacid-natrum. The CX3CR1 and NF-kB mRNA relative expression in mice sciatic nerve was significant decreased (P < 0.05) compared to model group which indicated that tashinone II A-sulfoacid-natrum can elevates the mechanical and thermal pain threshold through inhibiting the NF-kB and CX3CR1 expression in neuropathic cancer pain mice.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
 » References Top

1.
Harifi G, Amine M, Ait Ouazar M, Boujemaoui A, Ouilki I, Rekkab I, et al. Prevalence of chronic pain with neuropathic characteristics in the Moroccan general population: A national survey. Pain Med 2013;14:287-92.  Back to cited text no. 1
    
2.
Bouhassira D, Lantéri-Minet M, Attal N, Laurent B, Touboul C. Prevalence of chronic pain with neuropathic characteristics in the general population. Pain 2008;136:380-7.  Back to cited text no. 2
    
3.
Truini A, Cruccu G. Pathophysiological mechanisms of neuropathic pain. Neurol Sci 2006;27 Suppl 2:S179-82.  Back to cited text no. 3
    
4.
Urch CE, Dickenson AH. Neuropathic pain in cancer. Eur J Cancer 2008;44:1091-6.  Back to cited text no. 4
    
5.
Lin Y, Yufang L, Rui L, Yi G, Liang G. Effects of sulfotanshinone sodium injection on neuropathic pain in rats. Chinese Journal of Anesthesiology 2013;33:444-7.  Back to cited text no. 5
    
6.
Shimoyama M, Tanaka K, Hasue F, Shimoyama N. A mouse model of neuropathic cancer pain. Pain 2002;99:167-74.  Back to cited text no. 6
    
7.
Ochoa JL. Neuropathic pain: Redefinition and a grading system for clinical and research purposes. Neurology 2009;72:1282-3.  Back to cited text no. 7
    
8.
Treede RD, Jensen TS, Campbell JN, Cruccu G, Dostrovsky JO, Griffin JW, et al. Neuropathic pain: Redefinition and a grading system for clinical and research purposes. Neurology 2008;70:1630-5.  Back to cited text no. 8
    
9.
Baron R, Binder A, Wasner G. Neuropathic pain: Diagnosis, pathophysiological mechanisms, and treatment. Lancet Neurol 2010;9:807-19.  Back to cited text no. 9
    
10.
Eide PK, Rabben T. Trigeminal neuropathic pain: Pathophysiological mechanisms examined by quantitative assessment of abnormal pain and sensory perception. Neurosurgery 1998;43:1103-10.  Back to cited text no. 10
    
11.
Rosenthal P, Borsook D. Ocular neuropathic pain. Br J Ophthalmol 2016;100:128-34.  Back to cited text no. 11
    
12.
Khan N, Smith MT. Neurotrophins and neuropathic pain: Role in pathobiology. Molecules 2015;20:10657-88.  Back to cited text no. 12
    
13.
Dworkin RH, O'Connor AB, Backonja M, Farrar JT, Finnerup NB, Jensen TS, et al. Pharmacologic management of neuropathic pain: Evidence-based recommendations. Pain 2007;132:237-51.  Back to cited text no. 13
    
14.
Dworkin RH, O'Connor AB, Audette J, Baron R, Gourlay GK, Haanpää ML, et al. Recommendations for the pharmacological management of neuropathic pain: An overview and literature update. Mayo Clin Proc 2010;85 3 Suppl: S3-14.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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