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Plant-Derived Edible Nanoparticles in Cancer Drug Delivery
Published in Hala Gali-Muhtasib, Racha Chouaib, Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Siavash Iravani, Ghazaleh Jamalipour Soufi
In one study, grapefruit-derived nanovesicles were selectively taken up by intestinal macrophages and ameliorated dextran sulfate sodium-induced mouse colitis [12]. Their anti-inflammatory effects were mediated by up-regulating the expression of heme oxygenase-1 (HO-1) and inhibiting the productions of IL-1b and TNF-α in intestinal macrophages. It was demonstrated that these nanovesicles are biocompatible, biodegradable, and stable across a wide range of pH values, suggesting that they could be developed as an oral drug delivery system. Therefore, the anti-inflammatory drug methotrexate (MTX) was incorporated into grapefruit-derived nanovesicles. Consequently, it was found that the encapsulated drug showed a lower toxicity than free MTX and exhibited remarkably higher therapeutic effects against dextran sulfate sodium-induced colitis in mice. It was suggested that grapefruit-derived nanovesicles could serve as immune modulators in the intestine and promote homeostasis of intestinal macrophages. These NPs showed a potential for development as an oral delivery system for small molecule drugs aimed at attenuating inflammatory responses in human disease.
Pharmacotherapy of Neurochemical Imbalances
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rupali Patil, Aman Upaganlawar, Suvarna Ingale
It is a highly toxic gas when breathed in large amount. However, it also functions as a neurotransmitter. Its function in the brain is still being clarified. In neurons, enzyme heme oxygenase (HO) degrades heme to form biliverdin, iron, and finally CO. CO stimulates soluble guanylyl cyclase enzyme like NO. In enteric nervous system and olfactory receptor neurons, CO acts as strong neurotransmitter. The neurons of the myenteric plexus contain HO2 and neuronal nitric oxide synthase (nNOS) in abundant amount. Any genetic deletion or pharmacologic inhibition of HO2 considerably decreases noradrenergic neurotransmission in the gut. Similarly, there is reduction in the generation of cGMP in olfactory neurons due to inhibition of heme oxygenase, which normally produce adequate CO to stimulate guanylyl cyclase. Production of CO also plays an important role in the conservation of circadian rhythms by influencing the DNA binding activity of key circadian transcription factors (Nestler et al., 2009; Baranano et al., 2001).
Herbs with Antidepressant Effects
Published in Scott Mendelson, Herbal Treatment of Major Depression, 2019
Extracts of Eleutherococcus senticosus induce anti-neuroinflammatory and neuroprotective processes in cultured hippocampal and microglial cells through activation of Nrf2 and enhancement of HO-1 expression. These intracellular factors lie at the crux of oxidation and inflammation regulatory pathways. Nrf2 has a wide range of cytoprotective functions, including anti-oxidative stress, regulating glutathione synthesis, and anti-inflammatory effects. Heme oxygenase-1 serves as a powerful antioxidant, anti-inflammatory, and counter-agent to stresses of various types.8 Activation of these factors by Eleutherococcus senticosus reduce lipopolysaccharide-induced inflammatory, nitrosative and oxidative damage in hippocampal and microglial cells.9 Activation of the Nrf2/HO-1 signaling pathway in the brain is suspected of contributing to antidepressant effects.10
Iron metabolism and chronic inflammation in IgA nephropathy
Published in Renal Failure, 2023
Zhang-yu Tian, Zhi Li, Ling Chu, Yan Liu, Jin-rong He, Yu Xin, Ai-mei Li, Hao Zhang
Two functional isoforms of heme oxygenase exist in mammalian cells: HO-1 and HO-2. HO-2 is expressed in the brain, testis, cardiovascular and liver and can balance iron and redox metabolism as well as cellular messaging [158–160]. By contrast, HO-1 is a stress-inducible isozyme [161]. Under homeostatic conditions, HO-1 is constitutively expressed in iron-recycling macrophages in the spleen and liver and certain tolerogenic immune cells [162,163]. However, HO-1 is highly upregulated by most cells in response to free heme and many other pro-oxidants to provide protection against oxidative damage [140,141,164]. Micro and/or macroscopic hematuria is a typical symptom of IgAN that suggests potential induction of HO-1 in the glomeruli [165]. The HO-1 gene promoter length polymorphism was an important risk factor for mortality in IgAN [142].
Indomethacin: an exploratory study of antiviral mechanism and host-pathogen interaction in COVID-19
Published in Expert Review of Anti-infective Therapy, 2022
Nishant Shekhar, Harpinder Kaur, Phulen Sarma, Ajay Prakash, Bikash Medhi
Heme-oxygenase-1 (HMOX1) is the inducible isoform of heme-oxygenases (HO) that causes oxidative heme cleavage to biliverdine, carbon monoxide, and ferrous iron discharge, It has a regulatory role in intravascular inflammation activity [38]. Datillo (2020) using various studies, including Renieris (2020) explained that fatal SARS-CoV-2 infection leads to a very low level of serum H2S level in contrast to recovered cases [39,40]. In his model, Datillo proposed that SARS-CoV-2 infection downregulates HO-1 which leads to reduced heme breakdown, low CO concentration, which leads to low serum H2S concentration (HO-1/CO/H2S axis). Indomethacin is reported to consequently upregulate HO-1 levels in gastric mucosal cells of rats, according to Aburaya et al. (2006) [41]. In another gastric mucosal cell line study of rats, indomethacin was observed to reduce the indomethacin-induced mitochondrial oxidative stress (MOS) due to upregulation of HO-1 and prevention of MOS proinflammation [42]. These results point out the protective mechanism of HO-1 in response to oxidative stress and indomethacin-induced injury rather than directly modulating the HO-1 expression. The interaction of Orf3a with the HMOX1 gene might be associated with inhibition of HO-1 expression in SARS-CoV-2 infection since there is stated downregulation of HO-1 in SARS-CoV-2 affected individuals according to Datillo (2020). However, the effect of indomethacin in inducing HO-1 expression in SARS-CoV-2 infected patients remains undetermined.
ATF4-dependent heme-oxygenase-1 attenuates diabetic nephropathy by inducing autophagy and inhibiting apoptosis in podocyte
Published in Renal Failure, 2021
Shizhu Yuan, Xudong Liang, Wenfang He, Mingzhu Liang, Juan Jin, Qiang He
Heme oxygenase-1 (HO-1) is an essential enzyme in heme catabolism that has been shown to protect cells by inhibiting oxidative stress and apoptosis [23]. Previous studies have shown that ATF4 regulates HO-1 expression [24,25], however, role of ATF4/HO-1 pathway in regulating autophagy and apoptosis in DN is not defined. In the present study, we demonstrated that ATF4 regulates autophagy in DN podocytes by promoting HO-1 expression. siRNA mediated knockdown of ATF4 led to autophagy impairment and increased apoptosis in renal podocytes, which were partially rescued by mTORC1 inhibitor rapamycin and HO-1 overexpression in podocytes in vitro. Additionally, HO-1 agonist hemin treated DN mice showed marked reduction in albuminuria and renal damage accompanied by autophagy induction and reduced apoptosis in the kidney. Our present study utilizing in vitro and in vivo approaches shed light on the biology of ATF4/HO-1 pathway in regulating autophagy and apoptosis in renal podocytes in DN and suggests beneficial therapeutic effect of HO-1 agonist hemin in treating diabetic nephropathy.