Ba sil and its variou s species are known to ha ve an effect on common cold and possess immunomodulatory properties. This paper describes a clinical trial of a herbal formulation, Panchtulasi drops in acute common cold; the formulation consists of essential oils of five species of ocimum, namely; Ocimum sanctum Linn., Ocimum basilicum Linn., Ocimum gratissimum Linn., Ocimum citriodorum Linn. and Ocimum canum Linn.This was an open label, three arm Phase II study to determine the safety and effica cy of Panchatulasi drops in patients with acute common cold. The primary endpoint was reduction in symptoms of cold and number of days of illness. This was assessed using SF-8 and WURSS21 questionnaires. The secondary endpoint was changes in serum interleukin-8 and neutrophil count. The study duration was 8 days with telephonic follow-up on 10 th day. A total of 60 patients were randomized to treatment, placebo and a control (standard medication) in a radio of 2:1:1.The symptom severity, quality of life and number of days of illness measured by questionnaire was significantly reduced in the treatment arm between baseline and day 4 (p<0.05). The physical component score and overall health score of the SF-8 questionnaire also improved considerably in the treatment arm compared to placebo and control arms between baseline and day 4. However, mental component score did not improve significantly until day 6. Concentration of IL-8 did not show any statistically significant change in any of the study arms due to high variability. Neutrophil count, on the other hand, decreased in the treatment arm (p=0.0153) compared to placebo and control arms where it increased. Panchatulasi drops is an effective herbal remedy for common cold and can be used as an alternative to current treatments. There was a significant reduction in days of illness, severity of symptoms, and improvement in quality of life compared to placebo and control groups.
Mitochondria-associated ER membranes (MAM) are transient functional domains in the endoplasmic reticulum (ER) in close apposition to mitochondria involved in multiple metabolic functions, including the regulation of mitochondria functionality. Specifically, MAM interactions with mitochondria contribute to the regulation of mitochondrial dynamics, calcium transference between both organelles and the composition of mitochondrial membranes. In addition, recent data indicate that alterations in MAM-mitochondria contacts are associated with impairments in glucose metabolism and insulin resistance phenotypes, but the mechanism behind these defects is unknown. Human embryonic stem cell (ESC)-derived motor neurons (hMNs) and mouse models with pathogenic mutations in superoxide dismutase 1 (SOD1) have been shown to present with a progressive disruption of MAM structure and function, as it occurs in other models of amyotrophic lateral sclerosis (ALS). In this work, we have found that impairments in the activation of MAM in the context of SOD1 mutations, hinder the use of glucose-derived pyruvate as a mitochondrial fuel and trigger a shift in mitochondrial substrates from pyruvate to fatty acids. We also show that, over time, this change in mitochondrial fuels induces significant alterations in mitochondrial electron flow and in the active/de-active (A/D) status of complex I in mutant hMNs and spinal cord tissues, but not in brain. Our data agree with a role for MAM in the maintenance and regulation of cellular glucose metabolism and the selection of mitochondrial substrates and suggest that MAM disruption in ALS could be the underlying cause of the bioenergetic deficits observed in the disease.
Mitochondrial defects are a common hallmark of familial and sporadic forms of amyotrophic lateral sclerosis (ALS). However, the origin of these defects, including reduced pyruvate metabolism and reduced oxygen consumption, is poorly understood. These metabolic functions are regulated in specialized endoplasmic reticulum (ER) domains in close contact with mitochondria, called mitochondrial-associated ER membranes (MAM). Recently it has been shown that MAM domains are disrupted in ALS, but the connection between MAM dysregulation and mitochondrial defects in ALS cells remains unclear. Using human embryonic stem cell (ESC)-derived motor neurons (hMNs) and mouse models with ALS-pathogenic mutations in superoxide dismutase 1 (SOD1), we found that the glycolytic deficiency in ALS is a direct consequence of the progressive disruption of MAM structure and function that hinders the use of glucose-derived pyruvate as a mitochondrial fuel and triggers a shift in mitochondrial substrates from pyruvate to fatty acids. This glycolytic deficiency, over time, induces significant alterations in mitochondrial electron flow and in the active/dormant (A/D) status of complex I in spinal cord, but not in brain. These data agree with a role for MAM in the maintenance and regulation of cellular glucose metabolism and suggest that MAM disruption in ALS could be the underlying cause of the bioenergetic deficits observed in the disease.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.