ABSTRACT
Objective:To observe the analgesic effect of Panlongqi tablet（PLQT） on rats with chronic inflammatory pain， and to explore mechanism of the action preliminarily from the perspective of the nuclear factor kappa-light-chain-enhancer of activated B cells （NF-κB）and mitogen-activated protein kinase（MAPKs） signaling pathways. Method:Rats were induced to establish model of chronic inflammatory pain by complete Freund adjuvant（CFA）， which was divided into normal group， model group， the PLQT 0.16，0.32，0.64 g·kg-1 group， and the ibuprofen 0.05 g·kg-1 group（also positive group）， give the medicine once a day by gavage. Standard Von Frey fiber was used to evaluated the mechanical pain threshold， acetone was used to stimulated rats inflammatory foot to get the cold-induced response score， with the mechanical pain threshold and cold-induced response score to be observed at 1， 2， 3， 4 and 6 h before and after administration on day 1， and at 4 h after administration on day 3-7. The content of PGE2， IL-1， TNF-α in serum， inflammatory foot and 4-5 lumbar spinal cord was detected by enzyme-linked immunosorbent assay（ELISA）. The protein level of MAPKs （p-p38， p-ERK， p-JNK） in lumbar spinal cord 4-5 was detected by Western blot. The expression of NF-κB p65 in the lumbar spinal cord was detected by IFA. Result:Model group had lower mechanical pain threshold and higher cold-induced response score than these in normal group（P<0.01）， while the mechanical pain threshold and cold-induce response score of the model rats were dose-dependent better regulated after administration of PLQT 0.16， 0.32， 0.64 g·kg-1·d-1（P<0.05，P<0.01）， these effect lasted 6 h， of which PLQT groups get the most significant effect on 4 h， however the effect of IBP was similar to that of PLQT medium dose group. In addition， PLQT reduced the abnormal increase of PGE2， IL-1 and TNF-α contents in serum， inflammatory foot and spinal cord of rats in model group， decreased the protein phosphorylation levels of ERK and JNK in spinal cord， and decreased the protein expression of NF-κB p65， that was significant in the PLQT high-dose group（P<0.01）. Conclusion:PLQT had significant analgesic effect on chronic inflammatory pain model rats， which may be related to the inhibition of NF-κB and MAPKs signaling pathways in spinal cord.
ABSTRACT
Objective:To explore the compatibility of Panlongqi tablets in the treatment of osteoarthritis. Method:Network pharmacology was used to predict and screen the targets and pathways related to osteoarthritis of 59 compounds in Panlongqi tablets including activating blood circulation and removing stasis group（ACRG），expelling wind-damp group（EWDG）and tonifying liver and kidney group（TLKG）. Through data integration analysis, the characteristics and compatibility rules of this prescription in preventing and treating osteoarthritis were analyzed. Result:The 59 compounds can act on 70 osteoarthritis(OA) related targets, mainly involving inflammatory stimulation response, cell proliferation, cell metabolism, immune regulation and other related processes. Pathway enrichment analysis involved inflammatory response, cartilage degeneration, immune regulation, bone metabolism and other related pathways. Conclusion:The three drugs play different regulatory roles in the pathogenesis of OA, such as inflammation, chondrocyte apoptosis and metabolism, extracellular matrix degradation, and bone metabolism. Among them, promoting blood circulation and removing blood stasis were mainly related to anti-inflammatory and analgesia, the wind-dampening group was mainly involved in regulating immunity and inflammation, and the liver-kidney group was more related to bone metabolism and chondrocyte apoptosis.