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Objective To explore the application of cancer pain standardized treatment in patients with lung cancer pain and clinical results.Methods 120 cases of lung cancer pain patients as the research object in Our hospital from April 2015 to June 2016,The patients were randomly divided into study group and control group,60 cases in each group,the patients in the control group were treated with routine therapy and nursing,and the patients in the study group were treated with normalized treatment and care of cancer pain,and then compared the two groups after treatment Pain status changes and adverse events and patient satisfaction statistics.Results There was no significant difference in pain status and VAS score between the two groups before treatment,but the pain status was relieved after treatment.The pain status of patients in the study group after standardized treatment of cancer pain changed significantly,the VAS score was lower than the control,the difference between the two groups was statistically significant(P<0.05).After treatment,the adverse events of the study group including non-on-time medication,syncope pressure sores and the incidence of self-mutilation or suicide were statistically significant And the difference was statistically significant(P<0.05).The satisfaction of the patients in the two groups showed that the satisfaction of the patients in the study group was significantly higher than that of the control group,The difference between groups was statistically significant(P<0.05).Conclusion The standardized treatment of cancer pain is effective in the treatment of patients with lung cancer pain.It can effectively relieve the pain and improve the quality of life and satisfaction of patients with lung cancer pain.It has broad clinical application and popularization value.
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Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in activation of astrocytes in midbrain periaqueductal gray (PAG) of rats with neuropathic pain.Methods A total of 72 pathogen-free male Sprague-Dawley rats,aged 9 weeks,weighing 160-200 g,were divided into 4 groups using a random number table:control group (group C,n =8),neuropathic pain group (group NP,n =40),dimethyl sulfoxide control group (group DS,n =12) and JNK inhibitor SP600125 group (group SP,n=12).Neuropathic pain was produced by chronic constriction injury (CCI).At 14 days after CCI,10 nmol JNK inhibitor SP600125 0.5 μl was intraperitoneally injected into the PAG in group SP,and 10％ dimethyl sulfoxide 0.5 μl was given instead in group DS.Eight rats were selected in group C,before CCI and at 3,7,14 and 21 days after CCI in group NP,and in DS and SP groups,and the mechanical pain threshold was measured before CCI,before administration on 14 days after CCI and at 30,45,60,75 and 90 min after administration.The rats in group C were sacrificed after the end of measurement of the mechanical pain threshold,and brains were removed for determination of phosphorylated JNK (p-JNK) and glial fibrillary acidic protein expression (by Western blot) in PAG region.The rats in group NP were sacrificed after the end of measurement of the mechanical pain threshold at each time point,and brains were removed for detection of p-JNK expression in PAG region.Four rats in DS and SP groups were sacrificed after the last measurement of the mechanical pain threshold at 45 min after administration,and brains were removed for determination of glial fibrillary acidic protein expression in PAG region.Results Compared with group C,the mechanical pain threshold was significantly decreased at each time point after CCI,and the expression of p-JNK was up-regulated at 7-21 days after CCI in group NP (P＜0.01).Compared with group DS,the mechanical pain threshold was significantly increased at 30 min after administration,and GFAP expression was down-regulated at 45 min after administration in group SP (P＜ 0.01).The mechanical pain threshold was significantly higher at 30-75 min after administration than before administration in group SP (P＜0.01).Conclusion The mechanism underlying activation of astrocytes in PAG is related to activating JNK in the rats with neuropathic pain.