The neuroprotective and anti-inflammatory effects of diltiazem in spinal cord ischaemia-reperfusion injury.

The protective effects of diltiazem were examined in a rabbit model of spinal cord ischaemia-reperfusion induced by infrarenal aortic occlusion for 30 min. In the diltiazem group (n = 6), an intravenous infusion (2 microg/kg per min) was started 10 min before ischaemia induction; normal saline solution was infused in the control group (n = 6). Neurological function was assessed using modified Tarlov criteria 24 h after surgery. Plasma samples were analysed for interleukin (IL)-6 and IL-10. Spinal tissue was analysed for malondialdehyde, nitric oxide and reduced glutathione activities. Tarlov scores of the diltiazem-treated rabbits indicated significantly improved hind-limb motor function compared with the control group. The diltiazem group also had better quantitative and qualitative histopathological findings. Diltiazem infusion significantly reduced IL-6 levels 3 and 24 h after reperfusion compared with the control group. The mean IL-10 level in the diltiazem group was significantly higher than in the control group 24 h after reperfusion. It is concluded that diltiazem has cytoprotective and anti-inflammatory properties, leading to reduced spinal cord injury.

Caffeic acid phenethyl ester accelerates cutaneous wound healing in a rat model and decreases oxidative stress.

BACKGROUND: Cutaneous injury causes a depression in antioxidant status, as reactive oxygen species (ROS) are produced in response to injury. AIM: To determine the effects of caffeic acid phenethyl ester (CAPE), an antioxidant and anti-inflammatory agent, on wound healing in rats. METHODS: In total, 40 male rats were divided into two groups: one group treated with CAPE (n = 20) and a second untreated control group (n = 20). A linear full-thickness incision was performed on the back of each rat and sutured. After incision, CAPE was given to the treatment group and saline to the control group. On days 1, 3, 7 and 14, five animals in each group were killed, and wound tissues dissected for biochemical and histopathological analysis. RESULTS: Wound tissues showed a significant increase in glutathione and nitric oxide levels, and a significant decrease in malondialdehyde levels and superoxide dismutase levels in the CAPE group compared with the control group. Histopathology of the wound tissues displayed rapid epithelium development in the CAPE group compared with the control group. CONCLUSION: This study has demonstrated that CAPE partly accelerates full-thickness wound healing by its antioxidant and ROS-scavenging capabilities.

Elevated cAMP levels reverse Brucella melitensis-induced lipid peroxidation and stimulate IL-10 transcription in rats.

Brucella species are able to survive and replicate within the phagocytic vacuole of macrophages that induce chronic infection in humans and domestic animals. The activation of oxidative bactericidal activity is one of the defense systems which protect the host from the toxic effects of pathogens. The aim of this study was to evaluate lipid peroxidation, NO production, antioxidative system and inflammation during a period of brucella infection in a rat model; in addition to investigate the role of elevated intracellular cyclic AMP on Brucella-induced events. Brucella significantly induced lipid peroxidation in plasma, liver and spleen by 3-5-fold at 7 days postinfection. NO concentration was significantly elevated in the liver and spleen while unchanged in plasma. Cyclic AMP elevating agent, rolipram, administration (1mg/kg/day i.p., 3 days) gradually suppressed lipid peroxidation and NO formation to the basal level in plasma and spleen whilst only a slight decrease was observed in liver. Brucella considerably decreased SOD activity in the liver and spleen, with rolipram restoring the enzyme activity in liver and activity in spleen being unchanged. Reverse transcriptase PCR analyses showed that Brucella melitensis does not alter TNF-alpha and IFN-gamma transcriptions in liver and spleen. The pathogen did not consistently induce nitric oxide synthase mRNA transcriptions in animals; even in those housed in the same group. IL-10 transcription was induced by rolipram in spleen but not in liver. Our results suggest that activation of the cAMP/PKA pathway suppressed lipid peroxidation and the elevated NO concentrations caused by B. melitensis. Moreover, rolipram induced anti-inflammatory cytokine IL-10 transcription and SOD activity, albeit in a tissue dependent manner.