alloin and Inflammation

Topics: Amino Acids; Animals; Apoptosis; Biomarkers; Choline Deficiency; Diet; Dietary Fats; Emodin; Gene Expression Regulation; Heme Oxygenase-1; Inflammation; Liver; Male; Membrane Proteins; Mice; Mice, Knockout; NF-E2-Related Factor 2; Non-alcoholic Fatty Liver Disease

Myocardial ischemia/reperfusion injury (I/RI) frequently incurs in acute myocardial infarction with high morbidity and mortality worldwide and is characterized with cardiomyocyte apoptosis and inflammatory response. Aloin is a major anthraquinone from Aloe species and fulfills pleiotropic protective functions in several disease models including hepatic injury. Nevertheless, the potential of aloin in MI/RI remains elusive. Intriguingly, aloin had modest cytotoxicity in H9c2 cardiomyocytes. Importantly, aloin dose-dependently ameliorated cell viability that was inhibited in response to simulated ischemia/reperfusion (SI/R) stimulation. Moreover, the enhanced apoptosis in cells under SI/R conditions were reduced after aloin treatment, concomitant with the decrease in pro-apoptotic Bax protein levels and increase in anti-apoptotic Bcl-2 protein expression. Of interest, aloin administration attenuated SI/R-induced oxidant stress by decreasing reactive oxygen species (ROS) production, lactate dehydrogenase (LDH), and malondialdehyde (MDA) release and increasing activity of anti-oxidant stress enzyme superoxide dismutase (SOD). Additionally, the elevated pro-inflammatory cytokine levels were counteracted after aloin treatment in cells under SI/R conditions, including TNF-α, IL-6, and IL-1β. Mechanically, aloin further enforced the activation of the NF-E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling. Noticeably, blockage of this pathway by si-Nrf2 transfection blunted aloin-mediated cardioprotective efficacy against SI/R-evoked oxidative stress injury and inflammatory response. Thus, these findings corroborate that aloin may antagonize SI/R-induced cardiomyocyte injury by attenuating excessive oxidative stress and inflammation, thereby endorsing its potential as a promising therapeutic agent against myocardial infarction.

Topics: Animals; Cell Line; Emodin; Heme Oxygenase-1; Inflammation; Myocytes, Cardiac; NF-E2-Related Factor 2; Oxidative Stress; Protective Agents; Rats; Reperfusion Injury

BACKGROUND Barbaloin is one of the main medicinal ingredients of aloe vera, which displays various anti-inflammatory and anti-apoptosis properties in several inflammatory and fibrotic diseases. Our study evaluated its efficacy against dextran sulfate sodium (DSS)-induced colitis in rats. MATERIAL AND METHODS Ulcerative colitis (UC) rat models were established in vivo, and after barbaloin treatment, body weight and inflammation index were measured. Additionally, the signaling mechanism by which barbaloin protects against UC was investigated using LPS-infected Caco-2 cells. RESULTS Barbaloin could significantly reverse UC-induced weight loss and colon injury. Further, it could effectively increase the mRNA expression of IL-4 and IL-10 in colon tissues, while decreasing the expression of IFN-γ, IL-6, IL-1ß, and TNF-alpha. Furthermore, it significantly enhanced UC-inhibited atresia band 1 (ZO-1), occludin, and E-cadherin, and was also found to activate the AMPK signaling pathway. Additionally, si-RAN-induced knockdown, and overexpression assay showed that barbaloin could inhibit the UC-enhanced MLCK signaling pathway by activating the AMPK signaling pathway. CONCLUSIONS Barbaloin can effectively inhibit inflammation and reverse epithelial barrier function to protect against UC, possibly via activation of the AMPK signaling pathway.

Topics: AMP-Activated Protein Kinases; Animals; Anthracenes; Caco-2 Cells; Cadherins; Colitis; Dextran Sulfate; Dextrans; Disease Models, Animal; Fluorescein-5-isothiocyanate; Humans; Inflammation; Inflammation Mediators; Intestinal Mucosa; Lipopolysaccharides; Male; Myosin-Light-Chain Kinase; Occludin; Organ Size; Rats, Wistar; Signal Transduction; Zonula Occludens-1 Protein

Numerous herbal-derived natural products are excellent anti-inflammatory agents. Several studies have reported that aloin, the major anthraquinone glycoside obtained from the

Topics: Animals; Anti-Inflammatory Agents; Apoptosis; Cell Survival; Cyclooxygenase 2; Cytokines; Disease Models, Animal; Emodin; Inflammation; Inflammation Mediators; Lipopolysaccharides; Macrophages; Mice; Models, Biological; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; Phosphorylation; Protein Transport; Signal Transduction; Transcription Factor RelA

The anti‑inflammatory effects of aloin, a bioactive ingredient extracted from Aloe vera, have been described previously. The present study aimed to assess these effects and explore the underlying molecular mechanisms. RAW264.7 cells were incubated with different doses of aloin (100, 150 and 200 µg/ml) and lipopolysaccharide (LPS; 100 ng/ml) for the indicated times. Then, inducible nitric oxide synthase (iNOS) and cyclooxygenase‑2 expression levels were detected by western blot analysis and reverse transcription polymerase chain reaction (RT‑PCR).The concentrations of inflammatory cytokines in the cell culture supernatant were determined by ELISA. Total nitric oxide (NO) assay and reactive oxygen species (ROS) kits were used to detect NO and ROS levels, respectively. Mitogen‑activated protein kinase, nuclear factor κB and Janus kinase‑signal transducer and activator of transcription (JAK‑STAT) pathway activation were verified by western blot analysis. Confocal and nucleocytoplasmic separation experiments were used to detect STAT nuclear translocation. It was identified that aloin decreased the level of LPS‑induced iNOS expression, inhibiting the release of interleukin (IL)‑1β, IL‑6, tumour necrosis factor‑α and NO dose‑dependently. Mechanistically, aloin suppressed LPS‑induced JAK1‑STAT1/3 activation and STAT1/3 nuclear translocation. Additionally, LPS‑induced ROS production was inhibited by aloin. Collectively, these data suggest that aloin attenuated LPS‑induced inflammation by inhibiting ROS‑mediated activation of the JAK1‑STAT1/3 signalling pathway, thereby inhibiting the nuclear translocation of STAT1/3 in RAW264.7 cells. The present study provides an experimental basis for the clinical application of aloin in inflammatory‑associated diseases.

Topics: Animals; Emodin; Inflammation; Janus Kinase 1; Lipopolysaccharides; Mice; RAW 264.7 Cells; Reactive Oxygen Species; STAT1 Transcription Factor; STAT3 Transcription Factor

Ultraviolet B (UVB) irradiation mainly affects biological tissues by inducing an increase in reactive oxygen species (ROS) production which leads to deleterious outcomes for the skin, including pain and inflammation. As a protective strategy, many studies have focused on the use of natural products. The aim of this study was to investigate the effects of Aloe saponaria on nociceptive, inflammatory, and oxidative parameters in a model of UVB-induced sunburn in adult male Wistar rats. Sunburned animals were topically treated with vehicle (base cream), 1% silver sulfadiazine (positive control) or A. saponaria (10%) once a day for 6days. UVB-induced nociception (allodynia and hyperalgesia), inflammation (edema and leukocyte infiltration) and oxidative stress (increases in H2O2, protein carbonyl levels and lipid peroxidation and a decrease in non protein thiol content) were reduced by both A. saponaria and sulfadiazine topical treatment. Furthermore, A. saponaria or its constituents aloin and rutin reduced the oxidative stress induced by H2O2 in skin homogenates in vitro. Our results demonstrate that topical A. saponaria treatment displayed anti-nociceptive and anti-inflammatory effects in a UVB-induced sunburn model, and these effects seem to be related to its antioxidant components.

Topics: Analgesics; Animals; Anti-Inflammatory Agents; Antioxidants; Chromatography, High Pressure Liquid; Disease Models, Animal; Emodin; Inflammation; Male; Oxidative Stress; Plant Extracts; Plant Leaves; Rats; Rats, Wistar; Saponaria; Silver Sulfadiazine; Skin; Sunburn; Time Factors; Ultraviolet Rays