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         The possible underlying anti-inflammatory mechanisms of diazepam on acute and chronic inflammation could be occurred at least at six levels. The first level, the anti-inflammatory effects of diazepam may be due to the stimulation of genes responsible for steroid synthesis, which is one of the best characterized functions of PBRs by the PBR agonist like diazepam where diazepam stimulates  steroid synthesis mainly in adrenal gland cells and also, in the placenta, testis and ovaries; by enhancing the translocation of cholesterol from the outer to inner mitochondrial membranes

         The second level could be explaining the significant reduction of the inflammation in adjuvant arthritis with diazepam treatment, where it was assuming that PBRs expression was down-regulated in the chondrocytes when rheumatoid arthritis developed and the expression of these receptors in the chondrocytes was restored and increased following the treatment with a PBR ligand as diazepam or 4'-chloro- diazepam and this may account for the preventative and therapeutic actions of these PBR ligands on the rheumatoid arthritis, where the progressive erosion of cartilage and bone destruction may occur through a PBR-mediated modulation of apoptosis in chondrocytes, where PBRs are characterized by the modulation and control of the apoptosis process and the PBR ligands exhibit a potent anti-apoptotic activities , thus limiting erosion of cartilage and bone destruction in arthritis and this hypothesis is consistent with the results of  who reported that the PBR ligands as 4-chloro-diazepam could be effective in the management of the rheumatoid arthritis in the mice.

        At The third level, the PBRs anti-inflammatory effects could be explained also by the modification of genes responsible for cytokines production and secretions. Indeed, cartilage destruction is a major characteristic of rheumatoid arthritis and is linked to aberrant cytokines and growth factor expression in affected tissues .   It is well known that, IL-1, IL-6, TNF-α and IFN-γ can affect chondrocytes function . IL-6 has been shown to boost progression from an initial inflammation to a chronic state . Diazepam treatment was found to reduce and to suppress macrophage secretions of IL-1, IL-6 and TNF-α . Also, the PBR ligands as 4'-chloro-diazepam reduces dramatically both IL-6 and IL-13 expression in the pleural exudation of mice injected with carrageenan . Our results were in agreement with results of recent study reported that diazepam and resveratrol, are possessing obvious potential anti-inflammatory effects comparable to that of sulfasalazine on dextran sulphate sodium model of colitis as demonstrated with a significant decrease in serum levels of IL-6, TNF-α, PGE2, increase in serum corticosterone, decrease in colonic rat tissue leucocytes count, MOP, MDA and with a significant marked increase in antioxidant enzymes CAT and SOD in colonic tissues of DSS-induced colitis rat group treated concomitantly with diazepam and resveratrol 

        The fourth level, a previous study was suggested an important role of NO on the effects of diazepam on CIPE, where these anti-inflammatory effects of diazepam reflect its direct action on the PBRs present in the endothelial cells of the microvascular ambient and / or on immune and inflammatory cells that migrated to the inflammatory site at the rat paw thus, leading to a decrease in NO generation by NO synthase, which leading to a decrease in CIPE 

        While in the fifth level, it was reported that there are functional and biochemical evidence for diazepam as a cyclic nucleotidephosphodiesterase type 4 inhibitor. It was found that inhibition of PDE-4 isoenzyme can elicit some anti-inflammatory effects . The effect of diazepam on phosphodiesterases especially PDE-4 could be also part of the mechanisms involved in some experimental and clinical effects of benzodiazepines which are not well understood. Interestingly, diazepam has some effects such as airway smooth muscle relaxation and hyperglycaemia which are shared by PDE-4 inhibitors  and also, it is known that diazepam inhibits antigen-induced eosinophil infiltration into guinea-pig conjunctiva  as well as , other immune cell functions such as phagocytosis of human polymorphonuclearleukocytes and monocytes or human natural killer cell activity. Lastly at the six levels, it was reported that calcium channel blockers (CCBs) reduce the CIPE in rats and was attributing this anti-inflammatory effect due to stimulation of the HPA axis by CCBs