pelargonidin and Disease-Models--Animal

Pelargonidin (PEL) is a well-known red pigment found in plants, and it has been reported to have important biological activities that are potentially beneficial for human health. This study was initiated to determine whether PEL could modulate renal functional damage in a mouse model of sepsis, and to elucidate the underlying mechanisms. The potential of PEL treatment to reduce renal damage induced by cecal ligation and puncture (CLP) surgery in mice was measured by assessment of serum creatinine, blood urea nitrogen (BUN), lipid peroxidation, total glutathione, glutathione peroxidase (GSH-Px) activity, catalase activity, and superoxide dismutase (SOD) activity. Treatment with PEL resulted in elevated plasma levels of BUN and creatinine, and of protein in urine in mice with CLP-induced renal damage. Moreover, PEL inhibited nuclear factor-κB activation and reduced the induction of nitric oxide synthase and excessive production of nitric acid. PEL treatment also reduced the plasma levels of interleukin-6 and tumor necrosis factor-α reduced lethality due to CLP-induced sepsis, increased lipid peroxidation, and markedly enhanced the antioxidant defense system by restoring the levels of SOD, GSH-Px, and catalase in kidney tissues. These results suggested that PEL protects mice against sepsis-triggered renal injury.

Topics: Animals; Anthocyanins; Antioxidants; Blood Urea Nitrogen; Catalase; Creatinine; Disease Models, Animal; Glutathione Peroxidase; Humans; Interleukin-6; Kidney; Kidney Diseases; Ligation; Lipid Peroxidation; Male; Mice, Inbred C57BL; NF-kappa B; Nitric Acid; Nitric Oxide Synthase; Phytotherapy; Plant Extracts; Sepsis; Superoxide Dismutase; Tumor Necrosis Factor-alpha

Transforming growth factor β induced protein (TGFBIp) is an extracellular matrix protein expressed in several cell types in response to TGF-β. TGFBIp is released by human umbilical vein endothelial cells (HUVECs) and functions as a mediator of experimental sepsis. Pelargonidin (PEL) is a well-known red pigment found in plants, and has been reported as having important biological activities that are potentially beneficial for human health. This study was undertaken to investigate whether PEL can modulate TGFBIp-mediated inflammatory responses in HUVECs and in mice. The anti-inflammatory activities of PEL were determined by measuring permeability, leukocyte adhesion and migration, and activation of proinflammatory proteins in TGFBIp-activated HUVECs and mice. In addition, the beneficial effects of PEL on survival rate in a mouse sepsis model were tested. We found that PEL inhibited TGFBIp-induced barrier disruption, expression of cell adhesion molecules and adhesion/transendothelial migration of neutrophils to human endothelial cells. PEL also suppressed TGFBIp-induced hyperpermeability and leukocyte migration in vivo. These results suggest that PEL possesses anti-inflammatory properties that result in inhibition of hyperpermeability, expression of cell adhesion molecules, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases.

Topics: Animals; Anthocyanins; Anti-Inflammatory Agents; Cell Adhesion; Cell Adhesion Molecules; Cell Movement; Cells, Cultured; Disease Models, Animal; Extracellular Matrix Proteins; Human Umbilical Vein Endothelial Cells; Humans; Leukocytes; Male; Mice; Mice, Inbred C57BL; Neutrophils; Permeability; Phytochemicals; Primary Cell Culture; Sepsis; Survival Rate; Transforming Growth Factor beta

Alzheimer's disease (AD) is a disorder with multiple pathophysiological causes, destructive outcomes, and no available definitive cure. Pelargonidin (Pel), an anthocyanin derivative, is an estrogen receptor agonist with little estrogen side effects. This study was designed to assess Pel memory enhancing effects on the a rat Amyloid Beta25-35 (Aβ) intrahippocampal microinjections model of AD in the passive avoidance task performance paradigm and further evaluate the potential estrogen receptor role on the memory-evoking compound. Equally divided rats were assigned to 5 groups of sham, Aβ intrahippocampal microinjected, Pel pretreated (10 mg/kg; P.O), α estrogen antagonist intra-cerebrovascular (i.c.v.) microinjected, and β estrogen antagonist (i.c.v) microinjected animals. Intrahippocampal microinjections of Aβ were adopted to provoke AD model. Passive avoidance task test was also used to assess memory performance. Pel pretreatment prior to Aβ microinjections significantly improved step-through latency (P<0.001) in passive avoidance test. In α and β estrogen, antagonists received animals, passive avoidance task performance was not statistically changed (P=0.11 & P=0.41 respectively) compared to Pel pretreated and sham animals. Our results depicted that Pel improves Aβ induced memory dysfunction in passive avoidance test performance through estrogen receptor independently related pathways.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Anthocyanins; Avoidance Learning; Disease Models, Animal; Hippocampus; Male; Memory; Rats; Rats, Wistar; Receptors, Estrogen; Task Performance and Analysis

Alzheimer's disease (AD) is a multifactorial disorder with devastating outcomes and few mostly palliative available therapeutic strategies. Pelargonidin (Pel), an anthocyanin compound, is an estrogen receptor agonist with lower side effects versus estrogen. This study examined neuroprotective effect of Pel on intrahippocampal amyloid β25-35 (Aβ) rat model of AD. Rats were divided into groups of sham, Aβ, and Pel-pretreated Aβ (10mg/kg; p.o.). Animals underwent Morris water maze (MWM) test in addition to measurement of hippocampal oxidative stress, acetylcholinesterase (AChE) activity, glial fibrillary acidic protein (GFAP) and inducible nitric oxide synthase (iNOS). Pel pretreatment of Aβ group significantly improved escape latency and distance swum in MWM versus Aβ group and attenuated hippocampal malondialdehyde (MDA) and increased catalase activity with no significant change of nitrite. Meanwhile, Pel improved hippocampal AChE activity and lowered GFAP level with no significant change of iNOS. Our results suggest that Pel could improve Aβ25-35-induced memory deficit through mitigation of oxidative stress, cholinergic dysfunction, and astrocyte reaction.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Anthocyanins; Catalase; Cholinesterases; Disease Models, Animal; Glial Fibrillary Acidic Protein; Hippocampus; Male; Malondialdehyde; Memory Disorders; Neuroglia; Nitric Oxide Synthase Type II; Nitrites; Oxidative Stress; Peptide Fragments; Rats, Wistar; Reaction Time

Parkinson's disease (PD) is a neuropathological and debilitating disorder involving the degeneration of mesencephalic dopaminergic neurons. Neuroprotective effect of pelargonidin (Pel) has already been reported, therefore, this study examined whether Pel administration would attenuate behavioural and structural abnormalities and markers of oxidative stress in an experimental model of PD in rat. For this purpose, unilateral intrastriatal 6-hydroxydopamine (6-OHDA, 12.5mug/5mul of saline-ascorbate)-lesioned rats were pre-treated p.o. with Pel (10 and/or 20mg/kg). Pel administration dose-dependently attenuated the rotational behavior in lesioned rats and protected the neurons of SNC against 6-OHDA toxicity. In addition, pre-treatment with Pel (20mg/kg) significantly decreased the 6-OHDA-induced thiobarbituric acid reactive substances (TBARS) formation, indicative of a neuroprotection against lipid peroxidation. Furthermore, the increase of nitrite levels induced by 6-OHDA, indicate the nitric oxide formation and free radicals production and the decrease of antioxidant defense enzyme superoxide dismutase (SOD) was non-significantly prevented by Pel (20mg/kg). In summary, Pel administration has a dose-dependent neuroprotective effect against 6-OHDA toxicity, partly through attenuating oxidative stress. Our findings suggest that pelargonidin could provide benefits, along with other therapies, in neurodegenerative disorders including PD.

Topics: Administration, Oral; Animals; Anthocyanins; Antiparkinson Agents; Apomorphine; Cell Count; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Interactions; Functional Laterality; Lipid Peroxidation; Male; Mesencephalon; Neurons; Neuroprotective Agents; Nitric Oxide; Oxidopamine; Parkinsonian Disorders; Rats; Rats, Wistar; Statistics, Nonparametric; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances