Protective Effects of Liu Wei Di Huang Wan on the Liver, Orbitofrontal Cortex Nissl Bodies, and Neurites in MSG+PH-Induced Liver Regeneration Rat Model

Introduction. To examine the protective effects of Liu Wei Di Huang Wan formula (LWDH) on liver and orbitofrontal cortex (OFC) injuries in monosodium glutamate (MSG) and partial hepatectomy (PH) rat model. Methods. Neonatal Wistar rats were given MSG or saline on postnatal days 2, 4, 6, 8, and 10. The rats were caged into five groups and treated accordingly at six weeks old as follows: Saline group, Saline+PH group, MSG group, MSG+PH group, and LWDH group (MSG+PH+LWDH). The PH was performed during week 8 by excision of the left and median hepatic lobes (occupying about 68% of whole liver).On day 8 after the PH, the rats were subjected to an inner OFT before being sacrificed. The liver and OFC were stained using H&E, ORO, or Nissl staining. The expression of neurotrophic factors (β-NGF, BDNF) was examined in the OFC lysates by ELISA. Serum levels of cytokines (IL-1β, VEGF) were examined using the Bio-Plex suspension array. Results. LWDH increased the total distance traveled by the animals (p<0.05), and LWDH improved the integrity of the Nissl bodies in the OFC (mean area of the Nissl bodies, p<0.01; mean diameter, p<0.05; mean density, p<0.05; and IOD, p<0.01). There were less white area in the liver (p>0.05) and decreased hepatic steatosis (p<0.01) in LWDH group. LWDH administration decreased the expression of serum levels of IL-1β (p>0.05), while it increased VEGF (p>0.05) expression. LWDH administration increased the expression of BDNF (p>0.05) and β-NGF (p>0.05) in the OFC, all as compared to the MSG+PH group. Conclusion. LWDH partly protected the animals from depressive-like behaviors in the MSG+PH-induced liver regeneration neonatal rat model. LWDH alleviated hepatic injury and steatosis and, furthermore, protected the Nissl body integrity and the growth of neurites.

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Protective Effects of Platelet-Activating Factor Antagonist ABT-491 on the Peripheral Nerves in Hypoxic Ischemia-Induced Neonatal Rat Model

Turkiye Klinikleri Journal of Medical Sciences ◽

10.5336/medsci.2010-21244 ◽

2011 ◽

Vol 31 (5) ◽

pp. 1179-1185

Author(s):

Belgin BÜYÜKAKILLI ◽

Aytuğ ATICI ◽

Zekeriya BÜYÜKDERELİ ◽

Bahar TAŞDELEN ◽

Sevgi GÜNEŞ ◽

...

Keyword(s):

Rat Model ◽

Peripheral Nerves ◽

Platelet Activating Factor ◽

Neonatal Rat ◽

Protective Effects ◽

Hypoxic Ischemia ◽

Factor Antagonist ◽

Neonatal Rat Model

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Thrombopoietin Has Protective Effect in Neonatal Hypoxia-Ischemia Rat Model

Blood ◽

10.1182/blood-2019-131575 ◽

2019 ◽

Vol 134 (Supplement_1) ◽

pp. 4898-4898

Author(s):

Liang Li ◽

Liuming Yang ◽

Hongwu Xin ◽

Beng H Chong ◽

Mo Yang

Keyword(s):

Membrane Potential ◽

Protective Effect ◽

Brain Damage ◽

Mitochondrial Membrane Potential ◽

Rat Model ◽

Mitochondrial Membrane ◽

Conflicts Of Interest ◽

Neonatal Rat ◽

Neural Cells ◽

Protective Effects

Thrombopoietin (TPO) is a growth factor for the megakaryocytic lineage. The expression of TPO and TPO receptor (c-mpl) in the central nervous system (CNS) and the role of TPO in neural cells and brain damage models were investigated. Our results showed the expression of TPO in human cerebral hemisphere, cerebellum, cerebrospinal fluid and blood plasma. We found that TPO had a protective effect in hypoxic-ischemic rat model, as indicated by the increased ipsilateral brain weight and neuron density in a neonatal rat model of hypoxic-ischemic brain damage. Recoveries of sensorimotor functions and histopathology were observed in these animals that received TPO. In addition, TPO could promote C17.2 cells proliferation by activating PI3K/Akt signaling pathway, and the proliferation could be reduced to nearly basal level by the pre-treatment with LY 294002. The phosphorylation of AKT, which is a hallmark of activation of each molecule was significantly enhanced after the treatment with TPO in the cells, peaking at 30 min after stimulation with TPO. TPO was also found to have an anti-apoptotic effect which mediated via Bcl-2/BAX and suppressing the mitochondrial membrane potential. Results showed the increased level of Bcl-2 and decreased level of BAX were in the time-dependence manner (0, 5, 15, 30 and 60 mins) in these cells. In addition, the mitochondrial membrane potential was significantly decreased by adding 100 ng/ml TPO. Our results indicated that TPO have neural protective effects. Disclosures No relevant conflicts of interest to declare.

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Nitric Oxide Mediates Cerebral Ischemic Tolerance in a Neonatal Rat Model of Hypoxic Preconditioning

Journal of Cerebral Blood Flow & Metabolism ◽

10.1097/00004647-199903000-00011 ◽

1999 ◽

Vol 19 (3) ◽

pp. 331-340 ◽

Cited By ~ 174

Author(s):

Jeffrey M. Gidday ◽

Aarti R. Shah ◽

Raymond G. Maceren ◽

Qiong Wang ◽

Dale A. Pelligrino ◽

...

Keyword(s):

Nitric Oxide ◽

Rat Model ◽

Ischemic Tolerance ◽

Hypoxic Preconditioning ◽

Neonatal Rat ◽

No Production ◽

Protective Effects ◽

Nos Inhibitor ◽

Neuronal Nos ◽

Inducible Nos

Neuroprotection against cerebral ischemia can be realized if the brain is preconditioned by previous exposure to a brief period of sublethal ischemia. The present study was undertaken to test the hypothesis that nitric oxide (NO) produced from the neuronal isoform of NO synthase (NOS) serves as a necessary signal for establishing an ischemia-tolerant state in brain. A newborn rat model of hypoxic preconditioning was used, wherein exposure to sublethal hypoxia (8% oxygen) for 3 hours renders postnatal day (PND) 6 animals completely resistant to a cerebral hypoxic-ischemic insult imposed 24 hours later. Postnatal day 6 animals were treated 0.5 hour before preconditioning hypoxia with the nonselective NOS inhibitor L-nitroarginine (2 mg/kg intraperitoneally). This treatment, which resulted in a 67 to 81% inhibition of calcium-dependent constitutive NOS activity 0.5 to 3.5 hours after its administration, completely blocked preconditioning-induced protection. However, administration of the neuronal NOS inhibitor 7-nitroindazole (40 mg/kg intraperitoneally) before preconditioning hypoxia, which decreased constitutive brain NOS activity by 58 to 81%, was without effect on preconditioning-induced cerebroprotection, as was pretreatment with the inducible NOS inhibitor aminoguanidine (400 mg/kg intraperitoneally). The protective effects of preconditioning were also not blocked by treating animals with competitive [3-(2-carboxypiperazin-4-yl)propyl-1-phosphonate; 5 mg/kg intraperitoneally] or noncompetitive (MK-801; 1 mg/kg intraperitoneally) N-methyl-D-aspartate receptor antagonists prior to preconditioning hypoxia. These findings indicate that NO production and activity are critical to the induction of ischemic tolerance in this model. However, the results argue against the involvement of the neuronal NOS isoform, activated secondary to a hypoxia-induced stimulation of N-methyl-D-aspartate receptors, and against the involvement of the inducible NOS isoform, but rather suggest that NO produced by the endothelial NOS isoform is required to mediate this profound protective effect.

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Effects of Combined Anisodamine and Neostigmine Treatment on the Inflammatory Response and Liver Regeneration of Obstructive Jaundice Rats after Hepatectomy

BioMed Research International ◽

10.1155/2014/362024 ◽

2014 ◽

Vol 2014 ◽

pp. 1-9 ◽

Cited By ~ 3

Author(s):

Chong-Hui Li ◽

Xuan Zhang ◽

Xin-Lan Ge ◽

Xin Huang ◽

Ai-Qun Zhang ◽

...

Keyword(s):

Obstructive Jaundice ◽

Inflammatory Response ◽

Liver Regeneration ◽

Partial Hepatectomy ◽

Neutrophil Infiltration ◽

Serum Levels ◽

Saline Group ◽

Mrna Levels ◽

Ki 67 ◽

Duct Ligation

Background. Cholestasis is associated with high rates of morbidity and mortality in patients undergoing major liver resection. This study aimed to evaluate the effects of a combined anisodamine and neostigmine (Ani+Neo) treatment on the inflammatory response and liver regeneration in rats with obstructive jaundice (OJ) after partial hepatectomy.Materials and Methods. OJ was induced in the rats by bile duct ligation. After 7 days biliary drainage and partial hepatectomy were performed. These rats were assigned to a saline group or an Ani+Neo treatment group. The expressions of inflammatory mediators, liver regeneration, and liver damage were assessed at 48 h after hepatectomy.Results. The mRNA levels of TNF-α, IL-1β, IL-6, MCP-1, and MIP-1α, in the remnant livers, and the serum levels of TNF-αand IL-1βwere substantially reduced in the Ani+Neo group compared with saline group(P<0.05). The Ani+Neo treatment obviously promoted liver regeneration as indicated by the liver weights and Ki-67 labeling index(P<0.05). The serum albumin andγ-GT levels and liver neutrophil infiltration also significantly improved in the Ani+Neo group(P<0.05)compared with the saline group.Conclusions. These results demonstrate that the combined anisodamine and neostigmine treatment is able to improve the liver regeneration in rats with OJ by substantially alleviating the inflammatory response.

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The protective effects of Anakinra in a neonatal rat model of necrotizing enterocolitis

TURKISH JOURNAL OF MEDICAL SCIENCES ◽

10.3906/sag-2103-275 ◽

2021 ◽

Keyword(s):

Necrotizing Enterocolitis ◽

Rat Model ◽

Neonatal Rat ◽

Protective Effects ◽

Neonatal Rat Model

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Rh-relaxin-2 Attenuates Degranulation of mast cells by Inhibiting NF-κB through PI3K-AKT/TNFAIP3 Pathway in an Experimental Germinal Matrix Hemorrhage Rat Model

10.21203/rs.3.rs-27605/v1 ◽

2020 ◽

Author(s):

Peng Li ◽

Gang Zhao ◽

Fanfan Chen ◽

Yan Ding ◽

Tianyi Wang ◽

...

Keyword(s):

Mast Cells ◽

Rat Model ◽

Protective Effects ◽

Nissl Staining ◽

Germinal Matrix ◽

Germinal Matrix Hemorrhage ◽

Pi3k Inhibitor Ly294002 ◽

Neurobehavioral Function ◽

Phosphorylated Akt ◽

Relaxin 2

Abstract Background: Mast cells play an important role in early immune reactions in the brain by inducing degranulation and releasing inflammatory mediators. Our aim of the study is to investigate the effects of rh-relaxin-2 on mast cells and the underlying mechanisms in a GMH rat model. Methods: One hundred and sixty-four P7 rat pups were subjected to germinal matrix hemorrhage (GMH) by an intraparenchymal injection of bacterial collagenase. Clodronate liposome was administered through intracerebroventricular (i.c.v.) injections 24 hours prior to GMH to inhibit microglia. Rh-relaxin-2 was administered intraperitoneally at 1 hour and 12 hours after GMH. Small interfering RNA of RXFP1 and PI3K inhibitor LY294002 were given by i.c.v. injections. Post-GMH evaluation included neurobehavioral function, Western blot analysis, immunofluorescence, Nissl staining, and Toluidine staining. Results: Our results demonstrated that endogenous relaxin-2 was downregulated and that RXFP1 level peaked on the first day after GMH. Administration of rh-relaxin-2 improved neurological functions, attenuated degranulation of mast cells and neuroinflammation, and ameliorated post-hemorrhagic hydrocephalus after GMH. These effects were associated with RXFP1 activation, increased expression of PI3K, phosphorylated AKT and TNFAIP3, and decreased levels of phosphorylated NF-κB, tryptase, chymase, IL-6 and TNF-α. However, knockdown of RXFP1 and PI3K abolished the protective effects of rh-relaxin-2. Conclusions: Our findings showed that rh-relaxin-2 attenuated degranulation of mast cells and neuroinflammation, improved neurological outcomes and ameliorated hydrocephalus after GMH through RXFP1/PI3K-AKT/TNFAIP3/NF-κB signaling pathway.

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