Barrier In Rat Model Research Articles

Effect of berberine on the hippocampal structure, biochemical factors, memory, and blood-brain barrier in rat model of transient global cerebral ischemia.

Global cerebral ischemia (GCI) results in damage to the neurons and leads to cognitive impairments. Berberine (BBR) is known for its neuroprotective qualities. This study aimed to investigate the effects of BBR on memory, Blood-brain barrier (BBB) permeability, biochemical factors, and neuronal structure. Sixty-three adult male Wistar rats were divided randomly into Sham (21), GCI (21), and GCI + BBR (21) groups. The GCI + BBR group received 50 mg/kg of BBR for 7 days before and 6 h after 20 min of GCI induction. After 24 h, assessments included hippocampal neuronal structure, catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPX) levels, memory performance, and BBB permeability. The GCI + BBR group reduced volume loss in the CA1 and its sublayers (oriens, pyramidal, and radiatum) compared to the GCI group (p < 0.0001, p < 0.001, p < 0.01 and p < 0.001, respectively). Additionally, the GCI + BBR group showed higher pyramidal neuron density (p < 0.0001) and number (p < 0.0001) compared to the GCI group. BBR also decreased MDA levels (p < 0.0001) and increased CAT activity (p < 0.0001) in the GCI + BBR group compared to the GCI group, with GPX and SOD activity approaching Sham levels (p < 0.0001, both). BBR demonstrated significant improvements in short and long-term memory compared to the GCI group (p < 0.01, p < 0.0001, respectively). Furthermore, BBB permeability in the GCI + BBR group was significantly reduced compared to the GCI group (p < 0.0001). These findings demonstrated BBR's potential to protect the neurons in the CA1 and BBB structures, enhance antioxidant activity, and alleviate GCI-induced memory impairments.

HIV1-Nef perturbs the integrity of blood testis barrier in rat model

ABSTRACT The blood-testis barrier is a specialized feature within the mammalian testis, located in close proximity to the basement membrane of seminiferous tubules. This barrier serves to divide the seminiferous epithelium into distinct basal and adluminal (apical) compartments. The selectivity of the BTB to foreign particles makes it a safe haven for the virus, and the high affinity of HIV for testis might lead to the vertical transmission of the virus. In the present study, recombinant HIV1-Nef (rNef) protein was injected intravenously to examine the effect of rNef on BTB. SD male rats received 250 µg and 500 µg of rNef along with 2% Evans blue dye within 1 ml through the tail vein. After 1 hour of perfusion, the animals were sacrificed for analysis. The dye migration assay and ELISA confirmed a significant impairment in the blood-testis barrier (BTB) and the manifestation of rNef in testes tissues, respectively. Moreover, a decline in the expression of tight junction proteins, including ZO1 and Occludin, was observed during rNef-induced BTB disruption. Overall, our findings demonstrated that rNef induces BTB disruption through various signaling events. At the site of ectoplasmic specialization of the seminiferous epithelium, the localization of cadherins was found to be disrupted, making the testis a vulnerable site. In conclusion, rNef perturbs the integrity of the blood-testis barrier in rat models; hence, it can also serve as a suitable model for studying the dynamics of the blood-testis barrier.

Carbachol protects the intestinal barrier in severe acute pancreatitis by regulating Cdc42/F-actin cytoskeleton.

The present study aimed to investigate the effect of carbachol on the intestinal tight-junction barrier in a rat model of severe acute pancreatitis (SAP) without aggravating pancreatic injury, and to determine whether cell division cycle 42 (Cdc42)/F-actin could have a regulatory role. Rats were separated into a sham-operation (SO) group (n=10), SO + carbachol group (n=10), SAP group (n=60) and SAP + carbachol group (n=60). Sodium taurocholate (5%) was retrogradely injected into the biliopancreatic duct of rats to induce SAP. Subsequently, 16S rRNA sequencing was used to detect bacterial translocation (BT) in the gut of surviving animals. Hematoxylin and eosin staining was used to detect morphological changes in the pancreas and intestine. The expression of F-actin and tight junction proteins was analyzed by western blotting and immunofluorescence, and Cdc42 expression was analyzed by immunohistochemistry and western blotting. The results demonstrated that the intestinal injury in SO and SO + carbachol groups was lower than that in the SAP + carbachol group (P<0.05); however, the intestinal injury was similar in the SO and SO + carbachol groups (P>0.05), and was significantly more severe in the SAP group compared with the SAP + carbachol group (P<0.05). Similarly, pancreatic injury in the SAP and SAP + carbachol groups was significantly higher compared with the SO and SO + carbachol groups (P<0.05); however, pancreatic injury was similar in the SAP and SAP + carbachol groups (P>0.05), and in the SO and SO + carbachol groups (P>0.05). Furthermore, the mortality rate and BT in the SAP group were significantly higher compared with the SAP + carbachol group (mortality rate, 50% vs. 30%, P<0.05; BT, 60% vs. 33.3%, P<0.05). In addition, the expression of Cdc42, F-actin and claudin-2 was significantly higher in the SAP and SAP + carbachol groups compared with the SO and SO + carbachol groups (P<0.05), and the expression of occludin and zonula occludens-1 were significantly higher in the SO and SO + carbachol groups compared with the SAP and SAP + carbachol groups (P<0.05). In conclusion, these findings demonstrated that carbachol may protect the intestinal barrier in the SAP rat model without aggravating pancreatic injury via regulation of Cdc42/F-actin expression.

Effects of synbiotics on intestinal mucosal barrier in rat model

Summary Objective To investigate the protective effects of synbiotics on intestinal barrier function, and its priority to probiotics and prebiotics on intestinal barrier function in rat models. Methods We randomly divided 32 rats into four groups: control group (n = 8), probiotics group (n = 8), prebiotics group (n = 8) or synbiotics group (n = 8). All rats received cecectomy and gastrostomy, and tube feeding amoxicillin 50 mg and metronidazole 20 mg on operation day and the first operative day (POD1). After the establishment of impaired intestinal barrier model, rats in the 4 groups received intact protein enteral nutrition, intact protein enteral nutrition+ bifid-triple viable, intact protein enteral nutrition with dietary fiber, intact protein enteral nutrition with dietary fiber+ bifid-triple viable respectively. Samples of blood, urine and tissues of colonic mucose were collected on POD6. Thereafter we measured lactulose/mannitol (L/M) ratio, concentration of certain gut microflora, bacterial translocation rate, endotoxin level of portal vein serum and thickness of colonic mucose. Results Concentration of lactobacilli in probiotics group [(0.828 ± 0.366) × 107 CFU/g] and synbiotics group [(1.424 ± 0.928) × 107 CFU/g] were significantly higher than those in control group [(0.046 ± 0.037) × 107 CFU/g] and prebiotics group [(0.074 ± 0.046) × 107 CFU/g], P L/M ratio in synbiotics group (0.78 ± 0.43) was significantly lower than those in control group (1.45 ± 0.40), probiotics group (1.08 ± 0.22) and prebiotics group (1.35 ± 0.38), P Conclusions Probiotics can improve the concentration of colonic probiotics, while synbiotics can improve probiotics concentration and mucosa thickness in colon, decrease L/M ratio and bacterial translocation. Synbiotics shows more protective effects on intestinal mucosal barrier in rats after cecectomy and gastrostomy and the intervention of specific antibiotics.

Effects of salidroside pretreatment on expression of tumor necrosis factor-alpha and permeability of blood brain barrier in rat model of focal cerebralischemia-reperfusion injury

ObjectiveTo observe changes in expression of tumor necrosis factor (TNF)-alpha and permeability of blood brain barrier after salidroside pretreatment in rats with injury induced by focal cerebralischemia-reperfusion. MethodsForty-five male SD rats were randomly divided into three groups (n=15): control group, ischemia-reperfusion (IR) model group, and salidroside pretreatment group. Before the IR model establishment, the rats in the salidroside pretreatment group were intraperitoneally administered with salidroside at a dose of 24 mg/(kg·d) for 7 d. After 30 min post the last administration, the IR model was induced by occlusion of middle cerebral artery with a filament. After 24 h post the operation, the water content and Evens blue content in the ischemia cerebral hemisphere were determined, and the level of TNF-alpha mRNA was detected by the semi-quantitative RT-PCR. ResultsCompared with the IR model group, the salidroside pretreatment group had significantly lower (P<0.05) water content and Evens blue content in the ischemia cerebral hemisphere and also had significantly lower (P<0.05) level of TNF-alpha in the ischemic cerebral cortex tissue. ConclusionsThe salidroside pretreatment alleviated the focal cerebralischemia-reperfusion injury in the rat model, possibly by decreasing the permeability of blood brain barrier, attenuating brain edema and reducing TNF-alpha expression.

Assessment of processed human amniotic membrane as a protective barrier in rat model of sciatic nerve injury

Following nerve injury, scar formation is thought to be a considerable impediment to axonal regeneration at the nerve injury site. Nerve wrapping can protect the regenerating axons, and human amniotic membrane (HAM) derived from human placenta is an effective material for that purpose. The impact of nerve wrapping with HAM on functional recovery after nerve injuries, especially after autograft repair of long gap lesions, has not been comprehensively investigated. In the current study, we investigated whether the application of HAM as a nerve wrap to a 10 mm segment of transected and repaired nerve would reduce scar formation and permit better axonal regeneration and/or functional recovery in rats. The outcome was assessed with morphological and functional measures. We found that nerves wrapped with HAM had significantly fewer adhesions and less scar formation than controls. Although the final outcome, both functionally and morphologically, was not significantly improved by wrapping the nerve with HAM, the observed decrease in adhesions and scar formation might help the nerve retain its mobility and thus prevent traction injury and ischemia, which are caused by nerve tethering to the adjacent tissue during the healing process.