ants and Disease-Models--Animal

For many decades, the sting of Samsun ant (Pachycondyla sennaarensis) has been a serious clinical challenge for the people living in some of the major Middle East and Asian countries. In the present study, the therapeutic potential of Nigella sativa derived plant extract component, thymoquinone (TQ) has been tested against the Samsun ant venom (SAV) at the toxic dose in the rats.. The adult male rats were divided into four groups (n = 10): control, SAV treated, SAV + TQ treated and TQ alone treated. It was found that the sub-lethal dose of SAV alters not only many of the kidney and liver function markers but also induces oxidative stress in the animals. Moreover, the SAV also disturbs various immunological parameters including expression of PMNs, CD-80, CD-86, interleukins and other cytokines compromising the affected organism towards mild to severe allergic reactions including life-risking anaphylaxis.. The plant extract, TQ, effectively restores many of the biochemical and oxidative stress parameters comparable to the normal concomitant with improving the immunological aspects that might attributive in relieving from SAV-induced toxicity and allergic reactions in the affected organism to a greater extent.. Hence, TQ has an excellent antidote property against SAV-induced toxicities in vivo. Although the study is a vivid indication of the potential therapeutic potential of TQ against the SAV induced in vivo toxicity, yet the actual mechanism of interaction translating the toxicity amelioration warrants further investigations.

Topics: Acute Disease; Animals; Ant Venoms; Anti-Inflammatory Agents; Ants; B7-1 Antigen; B7-2 Antigen; Benzoquinones; Biomarkers; Disease Models, Animal; Immunity, Innate; Insect Bites and Stings; Kidney Function Tests; Liver Function Tests; Male; Nigella sativa; Plant Extracts; Rats; Rats, Wistar

Topics: Animals; Ant Venoms; Anticonvulsants; Ants; Bicuculline; Disease Models, Animal; Male; Mice; Seizures

Radix Salviae Miltiorrhizae, known as Danshen, is a well-known traditional Chinese herb which has been used extensively for the treatment of various diseases, including cardiovascular and cerebrovascular disease and neurodegenerative diseases for thousands of years. Tanshinone I is one of major bioactive flavonoids of Radix Salviae Miltiorrhizae. Modulation of microglial over-reaction may represent a therapeutic target to alleviate the progression of neurodegenerative diseases. Here, we tested the effect of Tanshinone I on neuro-inflammation and whether it can provide neuroprotection through inhibition of neuro-inflammation.. The effects of Tanshinone I on the production and/or mRNA expression of pro-inflammatory and anti-inflammatory factors in lipopolysaccharide(LPS)-induced BV-2 microglia cells were tested by Griess reaction, enzyme-linked immunosorbent assay (Elisa) or real time polymerase chain reaction. Activation of nuclear factor κ B (NF-κB) was measured by the nuclear translocation p65 and DNA binding activity. A model of Parkinson׳s disease was established by treatment of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6 mice. The effect of Tanshinone I on the behavioral changes, dopamine and its metabolites levels, expression of tyrosine hydroxylase (TH) and IBA-1, production of cytokines in the midbrain were investigated by the rotarod test, high-performance liquid chromatography (HPLC)-ECD, immunohistochemistry and Elisa. 1-methyl-4-phenylpyridinium (MPP+) concentration was tested by HPLC. Liver toxicity was determined by biochemical assay and histochemistry.. We found that the productions and/or expressions of several pro-inflammatory M1 factors such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 were highly suppressed by Tanshinone I in LPS-induced microglia. Interestingly, it did not affect the enhancement of expression of some anti-inflammatory M2 microglia markers, including IL-10, IL-1 receptor antagonist (IL-1Ra) and Cox-2. But it could significantly inhibit LPS-induced granulocyte colony-stimulating factor (G-CSF) expression. Tanshinone I could also inhibit LPS-induced NF-κB activation in microglia. Furthermore, it improved motor functions, normalized striatal neurotransmitters, and provided dopaminergic neuronal protection in MPTP-intoxicated mice. In vivo results also indicated that Tanshinone I could modulate MPTP-induced microglial activation, attenuated the increase of TNF-α, reserved the increase of IL-10 concentrain of MPTP-intoxicated mice. Tanshinone I does not alter MPTP toxic metabolite (MPP+) concentration. Oral administration of Tanshinone I at 10mg/kg daily for 2 weeks did not show liver toxicity.. Tanshinone I selectively suppressed pro-inflammatory M1 genes expression in activated microglia, interestingly, partially reserved anti-inflammatory M2 genes expression. It also could provide neuroprotection in a mouse model of Parkinson׳s disease. These data indicated that Tanshinone I could make the most of the beneficial side and minimize the detrimental side of activated microglia simultaneously, and provide neuroprotection by modulating the immune response of microglia.

Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Abietanes; Animals; Anti-Inflammatory Agents; Ants; Cell Line; Corpus Striatum; Cyclooxygenase 1; Cyclooxygenase 2; Cytokines; Disease Models, Animal; Gene Expression Regulation; Male; Membrane Proteins; Mice, Inbred C57BL; Microglia; Neuroprotective Agents; NF-kappa B; Nitric Oxide; Parkinsonian Disorders; Phytotherapy; Rotarod Performance Test

Arthropod venoms are potential sources of neuroactive substances, providing new tools for the design of drugs. The aim of this study was to evaluate the effects of Dinoponera quadriceps venom (DqV) on seizure models in mice induced by pentylenetetrazole (PTZ), pilocarpine, and strychnine. In the PTZ model, intraperitoneal treatment with DqV (0.5mg/kg) increased the time until the first seizure and the percentage of survival (155.4±27.7s/12.5%, p<0.05) compared to the control group (79.75±3.97s/0%), whereas endovenous treatment (0.1 and 0.5mg/kg) decreased the time until the first seizure (0.1mg/kg: 77.83±5.3s versus 101.0±3.3s in the control group; 0.5mg/kg: 74.43±3.9s versus 101.0±3.3s for the control group, p<0.05). We did not observe significant changes in the pilocarpine- and strychnine-induced seizure models. In assays that measured oxidative parameters in the PTZ model, intraperitoneal treatment with DqV (0.5 and 2.0mg/kg) only decreased the levels of MDA and nitrite in the cortex. However, endovenous treatment with DqV (0.1 and 0.5mg/kg) increased the levels of MDA in the cortex and hippocampus and at a dose of 0.5mg/kg in the striatum. Moreover, increased in nitrite content was observed in all three of the brain regions analyzed. Taken together, the D. quadriceps venom caused both neuroprotective and neurotoxic effects in a PTZ-induced seizure model, and this effect was dependent on the route of administration used.

Topics: Animals; Ant Venoms; Ants; Behavior, Animal; Disease Models, Animal; Male; Mice; Neuroprotective Agents; Seizures