scholarly journals The Restorative Effect of Red Guava (Psidium guajava L.) Fruit Extract on Pulmonary Tissue of Rats (Rattus norvegicus) Exposed to Cigarette Smoke

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Dewa Ketut Meles ◽  
Imam Mustofa ◽  
Wurlina Wurlina ◽  
Suherni Susilowati ◽  
Suzanita Utama ◽  
...  
Keyword(s):  
Cell Death ◽  
Cigarette Smoke ◽  
Rattus Norvegicus ◽  
Psidium Guajava ◽  
Cigarette Smoke Exposure ◽  
Fruit Extract ◽  
Pulmonary Tissue ◽  
Guava Fruit ◽  
Alveolar Tissue ◽  
Apoptosis And Necrosis

Since the damage to alveolar tissue due to cigarette smoke exposure (CSE) is lipid peroxidation, antioxidant treatment is needed. The red guava (Psidium guajava L.) fruit contains antioxidants derived from quercetin, lycopene, and vitamin C. This study aimed to determine the effect of red guava fruit extract (RGFE) on the alveolar tissue of rats exposed to cigarette smoke. The 25 rats (Rattus norvegicus) were divided into five groups. The control and T0 groups were only administered placebo, while T1, T2, and T3 groups were orally administered RGFE of 18.9, 37.8, and 56.7 mg/kg body weight daily for 44 days. The CSE dose of 20 suctions daily was conducted on T0, T1, T2, and T3 groups on days 15–44. On day 45, all rats were sacrificed for serum collection and histopathological lung slides with eosin-nigrosin staining. The result showed that CSE caused an increase p < 0.05 in malondialdehyde (MDA) levels, cell death, apoptosis, and necrosis percentages, congestion and thickening of alveolar septum tissue, and reduction in the alveolar diameter and alveolar number. Administration of RGFE suppressed those effects, and the highest dose of RGFE (T3) restored p > 0.05 MDA levels, percentage of apoptotic and necrosis, alveolar septal thickening, and alveolar diameter. However, the percentages of cell death, alveolar congestion, and the alveolar number were still worse p < 0.05 than in normal rats. It could be concluded that RGFE has proved relief and restoration of the alveolar tissue of rats exposed to cigarette smoke.

TRX-ASK1-JNK signaling regulation of cell density-dependent cytotoxicity in cigarette smoke-exposed human bronchial epithelial cells

2008 ◽  
Vol 294 (5) ◽  
pp. L921-L931 ◽  
Author(s):  
Yong Chan Lee ◽  
Chun-Yu Chuang ◽  
Pak-Kei Lee ◽  
Jin-Soo Lee ◽  
Richart W. Harper ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Cell Density ◽  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Bronchial Epithelial Cells ◽  
Air Pollutant ◽  
Cigarette Smoke Exposure ◽  
Bronchial Epithelial ◽  
Density Dependent

Cigarette smoke is a major environmental air pollutant that injures airway epithelium and incites subsequent diseases including chronic obstructive pulmonary disease. The lesion that smoke induces in airway epithelium is still incompletely understood. Using a LIVE/DEAD cytotoxicity assay, we observed that subconfluent cultures of bronchial epithelial cells derived from both human and monkey airway tissues and an immortalized normal human bronchial epithelial cell line (HBE1) were more susceptible to injury by cigarette smoke extract (CSE) and by direct cigarette smoke exposure than cells in confluent cultures. Scraping confluent cultures also caused an enhanced cell injury predominately in the leading edge of the scraped confluent cultures by CSE. Cellular ATP levels in both subconfluent and confluent cultures were drastically reduced after CSE exposure. In contrast, GSH levels were significantly reduced only in subconfluent cultures exposed to smoke and not in confluent cultures. Western blot analysis demonstrated ERK activation in both confluent and subconfluent cultures after CSE. However, activation of apoptosis signal-regulating kinase 1 (ASK1), JNK, and p38 were demonstrated only in subconfluent cultures and not in confluent cultures after CSE. Using short interfering RNA (siRNA) to JNK1 and JNK2 and a JNK inhibitor, we attenuated CSE-mediated cell death in subconfluent cultures but not with an inhibitor of the p38 pathway. Using the tetracycline (Tet)-on inducible approach, overexpression of thioredoxin (TRX) attenuated CSE-mediated cell death and JNK activation in subconfluent cultures. These results suggest that the TRX-ASK1-JNK pathway may play a critical role in mediating cell density-dependent CSE cytotoxicity.

scholarly journals Apoptosis and necrosis: two different outcomes of cigarette smoke condensate-induced endothelial cell death

2012 ◽  
Vol 3 (11) ◽  
pp. e424-e424 ◽  
Author(s):  
B Messner ◽  
S Frotschnig ◽  
A Steinacher-Nigisch ◽  
B Winter ◽  
E Eichmair ◽  
...  
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Cigarette Smoke ◽  
Cigarette Smoke Condensate ◽  
Endothelial Cell Death ◽  
Apoptosis And Necrosis

scholarly journals Guava (Psidium guajava) Fruit Extract Prepared by Supercritical CO2 Extraction Inhibits Intestinal Glucose Resorption in a Double-Blind, Randomized Clinical Study

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1512 ◽  
Author(s):  
Alice König ◽  
Bettina Schwarzinger ◽  
Verena Stadlbauer ◽  
Peter Lanzerstorfer ◽  
Marcus Iken ◽  
...  
Keyword(s):  
Psidium Guajava ◽  
Control Group ◽  
Supercritical Co2 Extraction ◽  
Fruit Extract ◽  
Guava Fruit ◽  
Glucose Levels ◽  
In Vivo Experiments ◽  
Randomized Clinical Study

Inhibition of intestinal glucose resorption can serve as an effective strategy for the prevention of an increase in blood glucose levels. We have recently shown that various extracts prepared from guava (Psidium guajava) inhibit sodium-dependent glucose cotransporter 1 (SGLT1)- and glucose transporter 2 (GLUT2)-mediated glucose transport in vitro (Caco-2 cells) and in vivo (C57BL/6N mice). However, the efficacy in humans remains to be confirmed. For this purpose, we conducted a parallelized, randomized clinical study with young healthy adults. Thirty-one volunteers performed an oral glucose tolerance test (OGTT) in which the control group received a glucose solution and the intervention group received a glucose solution containing a guava fruit extract prepared by supercritical CO2 extraction. The exact same extract was used for our previous in vitro and in vivo experiments. Blood samples were collected prior to and up to two hours after glucose consumption to quantitate blood glucose and insulin levels. Our results show that, in comparison to the control group, consumption of guava fruit extract resulted in a significantly reduced increase in postprandial glucose response over the basal fasting plasma glucose levels after 30 min (Δ control 2.60 ± 1.09 mmol/L versus Δ intervention 1.96 ± 0.96 mmol/L; p = 0.039) and 90 min (Δ control 0.44 ± 0.74 mmol/L versus Δ intervention −0.18 ± 0.88 mmol/L; p = 0.023). In addition, we observed a slightly reduced, but non-significant insulin secretion (Δ control 353.82 ± 183.31 pmol/L versus Δ intervention 288.43 ± 126.19 pmol/L, p = 0.302). Interestingly, storage time and repeated freeze-thawing operations appeared to negatively influence the efficacy of the applied extract. Several analytical methods (HPLC-MS, GC-MS, and NMR) were applied to identify putative bioactive compounds in the CO2 extract used. We could assign several substances at relevant concentrations including kojic acid (0.33 mg/mL) and 5-hydroxymethylfurfural (2.76 mg/mL). Taken together, this clinical trial and previous in vitro and in vivo experiments confirm the efficacy of our guava fruit extract in inhibiting intestinal glucose resorption, possibly in combination with reduced insulin secretion. Based on these findings, the development of food supplements or functional foods containing this extract appears promising for patients with diabetes and for the prevention of insulin resistance. Trial registration: 415-E/2319/15-2018 (Ethics Commissions of Salzburg).

scholarly journals Heme oxygenase-1-mediated autophagy protects against pulmonary endothelial cell death and development of emphysema in cadmium-treated mice

2015 ◽  
Vol 309 (3) ◽  
pp. L280-L292 ◽  
Author(s):  
Ranu Surolia ◽  
Suman Karki ◽  
Hyunki Kim ◽  
Zhihong Yu ◽  
Tejaswini Kulkarni ◽  
...  
Keyword(s):  
Cell Death ◽  
Lung Function ◽  
Cigarette Smoke ◽  
Heme Oxygenase ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Intratracheal Instillation ◽  
Cigarette Smoke Exposure ◽  
Heme Oxygenase 1 ◽  
Micro Computed Tomography

Pulmonary exposure to cadmium, a major component of cigarette smoke, has a dramatic impact on lung function and the development of emphysema. Cigarette smoke exposure induces heme oxygenase-1 (HO-1), a cytoprotective enzyme. In this study, we employed a truncated mouse model of emphysema by intratracheal instillation of cadmium (CdCl2) solution (0.025% per 1 mg/kg body wt) in HO-1+/+, HO-1−/−, and overexpressing humanized HO-1 bacterial artificial chromosome (hHO-1BAC) mice. We evaluated the role of HO-1 in cadmium-induced emphysema in mice by analyzing histopathology, micro-computed tomography scans, and lung function tests. CdCl2-exposed HO-1−/− mice exhibited more severe emphysema compared with HO-1+/+ or hHO-1BAC mice. Loss of pulmonary endothelial cells (PECs) from the alveolar capillary membrane is recognized to be a target in emphysema. PECs from HO-1+/+, HO-1−/−, and hHO-1BAC were employed to define the underlying molecular mechanism for the protection from emphysema by HO-1. Electron microscopy, expression of autophagic markers (microtubule-associated protein 1B-light chain 3 II, autophagy protein 5, and Beclin1) and apoptotic marker (cleaved caspase 3) suggested induction of autophagy and apoptosis in PECs after CdCl2 treatment. CdCl2-treated HO-1−/− PECs exhibited downregulation of autophagic markers and significantly increased cleaved caspase 3 expression and activity (∼4-fold higher). Moreover, hHO-1BAC PECs demonstrated upregulated autophagy and absence of cleaved caspase 3 expression or activity. Pretreatment of HO-1+/+ PECs with rapamycin induced autophagy and resulted in reduced cell death upon cadmium treatment. Induction of autophagy following CdCl2 treatment was found to be protective from apoptotic cell death. HO-1 induced protective autophagy in PECs and mitigated cadmium-induced emphysema.

scholarly journals Cadmium-mediated toxicity of lung epithelia is enhanced through NF-κB-mediated transcriptional activation of the human zinc transporter ZIP8

2012 ◽  
Vol 302 (9) ◽  
pp. L909-L918 ◽  
Author(s):  
Jessica R. Napolitano ◽  
Ming-Jie Liu ◽  
Shengying Bao ◽  
Melissa Crawford ◽  
Patrick Nana-Sinkam ◽  
...  
Keyword(s):  
Cell Death ◽  
Lung Disease ◽  
Cigarette Smoke ◽  
Critical Role ◽  
Zinc Transporter ◽  
Cigarette Smoke Exposure ◽  
Metal Exposure ◽  
Dependent Manner ◽  
Cell Toxicity ◽  
Cd Uptake

Cadmium (Cd), a toxic heavy metal and carcinogen that is abundantly present in cigarette smoke, is a cause of smoking-induced lung disease. SLC39A8 (ZIP8), a zinc transporter, is a major portal for Cd uptake into cells. We have recently identified that ZIP8 expression is under the transcriptional control of the NF-κB pathway. On the basis of this, we hypothesized that cigarette-smoke induced inflammation would increase ZIP8 expression in lung epithelia, thereby enhancing Cd uptake and cell toxicity. Herein we report that ZIP8 is a central mediator of Cd-mediated toxicity. TNF-α treatment of primary human lung epithelia and A549 cells induced ZIP8 expression, resulting in significantly higher cell death attributable to both apoptosis and necrosis following Cd exposure. Inhibition of the NF-κB pathway and ZIP8 expression significantly reduced cell toxicity. Zinc (Zn), a known cytoprotectant, prevented Cd-mediated cell toxicity via ZIP8 uptake. Consistent with cell culture findings, a significant increase in ZIP8 mRNA and protein expression was observed in the lung of chronic smokers compared with nonsmokers. From these studies, we conclude that ZIP8 expression is induced in lung epithelia in an NF-κB-dependent manner, thereby resulting in increased cell death in the presence of Cd. From this we contend that ZIP8 plays a critical role at the interface between micronutrient (Zn) metabolism and toxic metal exposure (Cd) in the lung microenvironment following cigarette smoke exposure. Furthermore, dietary Zn intake, or a lack thereof, may be a contributing factor in smoking-induced lung disease.

Effects of depletion of neutrophils or macrophages on development of cigarette smoke-induced emphysema

1999 ◽  
Vol 277 (1) ◽  
pp. L97-L105 ◽  
Author(s):  
A. Felix Ofulue ◽  
Mary Ko
Keyword(s):  
Cigarette Smoke ◽  
Lavage Fluid ◽  
Smoke Inhalation ◽  
Cigarette Smoke Exposure ◽  
Neutrophil Accumulation ◽  
Air Exposure ◽  
Specific Suppression ◽  
Cell Counts ◽  
Rabbit Igg ◽  
Alveolar Tissue

The aim of this study was to ascertain the putative roles of neutrophils or macrophages in the pathogenesis of cigarette smoking-induced emphysema on the basis of effects of anti-neutrophil (anti-PMN) antibody or anti-monocyte/macrophage (anti-MoMac) antibody on the development of emphysema in cigarette smoke-exposed rats. Rats were treated with rabbit anti-PMN or anti-MoMac antibody and exposed 7 days/wk for 2 mo to cigarette smoke inhalation; rats treated with nonimmunized rabbit IgG (control antibody) and exposed to cigarette smoke or normal room air served as controls. Antibody treatments began 24 h before the start of smoke or air exposure and was continued with 1 treatment/wk. Total and differential cell counts in bronchoalveolar lavage fluid and collagenase-dissociated lung and determinations of the elastinolytic activity of lung neutrophils or macrophages in [3H]elastin-coated wells indicated specific suppression of neutrophil accumulation and neutrophil-related elastinolytic burden in the lungs of the anti-PMN antibody-treated smoke-exposed rats, in contrast to specific suppression of macrophage accumulation and macrophage-related elastinolytic burden in the lungs of the anti-MoMac antibody-treated smoke-exposed rats. Cigarette smoke exposure-induced lung elastin breakdown (quantitated by immunologic assay of levels of elastin-derived peptides and desmosine in lavage fluid) and emphysema in the lungs (based on morphometric analysis of alveolar mean linear intercepts and alveolar tissue density in fixed lungs) were not prevented in the lungs of anti-PMN antibody-treated smoke-exposed rats but was clearly prevented in lungs of the anti-MoMac antibody-treated smoke-exposed rats. These findings implicate macrophages rather than neutrophils as the critical pathogenic factor in cigarette smoke-induced emphysema.

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