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1.
Int Immunopharmacol ; 113(Pt A): 109337, 2022 Dec.
Article in English | MEDLINE | ID: mdl-36274489

ABSTRACT

Inflammatory pain is the most important clinical symptom of inflammatory diseases. Despite intensive research into inflammatory pain mechanisms, the majority of analgesics available are based on mechanistic classes of compounds that have been known for many years, as a result, inflammatory pain control remains a challenge for drug design in the context of clinically unmet needs in terms of safety and efficacy. A growing literature supports that pro-inflammatory cytokine signaling plays a crucial role in the development of inflammatory pain. Modulation of the pro-inflammatory cytokine may hold the key to improved pain management. Previous studies have reported that dorsomorphin played key roles in inflammation. But the role of dorsomorphin in the formalin-induced inflammatory nociception in mice has never been reported. Here, we report a new function of dorsomorphin which can inhibit formalin-induced inflammatory nociception in mice. The antinociceptive effect of dorsomorphin mainly depended on inhibiting the p38 MAPK/c-fos signaling and regulating inflammatory mediators.


Subject(s)
Analgesics , Nociception , Mice , Animals , Pain Measurement , Analgesics/therapeutic use , Analgesics/pharmacology , Pain/drug therapy , Formaldehyde/pharmacology , Formaldehyde/therapeutic use , Cytokines/therapeutic use
2.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-451681

ABSTRACT

Objective To explore Wang Xingkuan’s rules of syndrome and treatment of chest blocking and heartache (Xiongbixintong).Methods Collection of professor Wang Xingkuan’s 267 consilia of patients with Xiongbixintong for outpatients. Chinese medicine terminology was regulated and Excelldatabase was established. Symptom, syndrome element, pathogenesis and treatment were statistically described by using Weka3.6 software, and Apriori algorithm was adopted for the main pathogenesis→treatment analysis of association rules.Results Symptoms include:chest pain, heart palpitations, shortness of breath, pale tongue (dark) red, etc. Syndrome elements include:in liver, and heart, and blood stasis, phlegm, qi stagnation, etc. The key pathogenesis is liver-heart imbalance, including stagnation of liver qi, heart and blood stasis, deficiency of heart qi-ying, disturbing heart-mind, etc. The principle of treatment is liver-heart Tongzhi, so the treatment is of“liver” with Shu gan-mu;treatment of“heart” contains freeing channels, eliminating phlegm and blood stasis, quiet the heart, replenishing qi-ying, etc. The main pathogenesis related credibility→treatment was higher than 0.50;with high reliability, the liver-heart imbalance→liver-heart Tongzhi was 0.71. Medication includes catharsis and tonic,“catharsis” to salvia, allium macrostemon, pseudo-ginseng, bupleurum, etc;“tonic” to white ginseng, ophiopogon japonicus, radix paeoniae alba, poria with hostwood, polygala tenuifolia, etc. Conclusion “Xintongzhigan, liver-heart Tongzhi, catharsis and tonic” is Wang Xingkuan’s thoughts and experience in treating Xiongbixintong.

3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-440152

ABSTRACT

Objective To observe the intervention effects of Xintongfang on the expression of P-selectin (PS), P-selectin glycoprotein ligand-1 (PSGL-1), platelet-leukocyte aggregates (PLA) and platelet-monocyte aggregates (PMA) in patients of coronary heart disease with carotid artery plaque. Methods Sixty patients were randomly divided into Xintongfang group and the control group, with 30 cases in each group. Xintongfang group was given Xintongfang, the control group was given aspirin and atorvastatin calcium for two months. The expression of PS, PSGL-1, PLA and PMA were tested by flow cytometry before and after treatment. Results The expression of PS, PSGL-1, PLA and PMA in two groups were reduced (P<0.01). Xintongfang group had more obvious effects on the expression of PLA and PMA than the control group (P<0.05). Conclusion Xintongfang can reduce the degree of inflammatory in patients of coronary heart disease with carotid artery plaque by inhibiting platelet-leukocyte interaction.

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