Column chromatography of the alcoholic extract of Piper betle roots furnished aristololactam A-II and a new phenyl propene, characterized as 4-allyl resorcinol, while the petroleum-ether extract yielded a diketosteroid, viz. stigmast-4-en-3,6-dione. All these compounds were characterized by spectroscopic means. Isolation of these compounds from this source is being reported here for the first time.
The current investigation has identified the biomarkers associated with severity of disability and correlation among plethora of systemic, cellular and molecular parameters of intellectual disability (ID) in a rehabilitation home. The background of study lies with the recent clinical evidences which identified complications in ID. Various indicators from blood and peripheral system serve as potential surrogates for disability related changes in brain functions. ID subjects (Male, age 10 ± 5 yrs, N = 45) were classified as mild, moderate and severe according to the severity of disability using standard psychometric analysis. Clinical parameters including stress biomarkers, neurotransmitters, RBC morphology, expressions of inflammatory proteins and neurotrophic factor were estimated from PBMC, RBC and serum. The lipid peroxidation of PBMC and RBC membranes, levels of serum glutamate, serotonin, homocysteine, ROS, lactate and LDH-A expression increased significantly with severity of ID whereas changes in RBC membrane β-actin, serum BDNF, TNF-α and IL-6 was found non-significant. Structural abnormalities of RBC were more in severely disabled children compared to mildly affected ones. The oxidative stress remained a crucial factor with severity of disability. This is confirmed not only by RBC alterations but also with other cellular dysregulations. The present article extends unique insights of how severity of disability is correlated with various clinical, cellular and molecular markers of blood. This unique study primarily focuses on the strong predictors of severity of disability and their associations via brain-blood axis.
The role of oleic acid as a protective antioxidant has recently been recognized. The present study is aimed to explore whether oleic acid can afford protection to rat gastric tissue when challenged with adrenaline. Sixty adult healthy male albino rats were divided into 10 groups comprising of 6 animals each. First group constituted the control. Rats of the second group were injected sub-cutaneously with adrenaline bitartrate at the dose of 0.3mg/kg body weight, every day for a period of 17 days. Rats of the third, to the sixth groups were orally fed with different doses of oleic acid (2.5, 5, 10, 20 mg/kg body weight/day) respectively. The rats of seventh to tenth groups were orally fed with doses of oleic acid as mentioned above and subsequently injected with adrenaline bitartrate at 0.3mg/kg body weight sub-cutaneously. After the treatment period, the animals were euthanized through cervical dislocation following light ether anaesthesia and gastric tissues were collected for morphological and biochemical studies. Subcutaneously administered pharmacological dose of adrenaline bitartrate caused oxidative stress inducing gastric lesion in male albino rats as evident from the altered levels of biomarkers of oxidative stress, activities of antioxidant and mitochondrial enzymes related to energy metabolism with changes in tissue morphology. Pre-treatment of rats with oleic acid dose-dependently protected against these gastric injuries induced by adrenaline indicating the potentiality of oleic acid in protecting against adrenaline induced gastric injury in male albino rats where antioxidant mechanisms appear to play a pivotal role in mediating such protection.
The present study explored efficient and exclusive analgesic effects of iboga-analogs in formalin-induced mouse via acute pain model. Novel iboga derivatives namely iboga-alcohol, iboga-amide, iboga-methylamide and iboga ester-exo were administered intraperitoneally to evaluate the anti-nociceptive, anti-inflammatory and neuromodulatory effects. Pain assessment was done by paw diameter, paw licking and tail immersion tests. Locomotor activity and anxiety-like behavior were determined by open field test and elevated plus maze. Inflammatory mediators, neurotransmitters and neurotrophic factors were measured from isolated serum, paw tissue and spinal segment. Iboga-analogs significantly reduced paw diameters. Decreased tail flick latency reversed in iboga-alcohol and methyl-amide particularly. Restricted locomotion was also significantly reversed in iboga-alcohol, iboga-amide, and iboga-methyl amide. Anxiolytic behaviour was obtained in the iboga-alcohol, iboga-amide and methyl-amide treated groups. Paw Substance P, CGRP, COX-2 and p65 nuclear translocation; serum IL-6 & TNF-α levels were significantly decreased in the iboga-alcohol treated group. Iboga-alcohol reversed the downregulation of GABA, Dopamine, and elevation of Substance P, NK1R and Glutamate. HRMS analysis confirmed the passage of all iboga-analogs in the brain. Iboga-analogs overturned the depleted BDNF whereas, GDNF elevation was further exaggerated. Taken together, these novel iboga-analogs, particularly iboga-alcohol, executed effective anti-nociception and prevented neuroinflammation. They warrant further clinical applications in acute pain situations.
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