Hydrogen protects against liver injury during CO2 pneumoperitoneum in rats

Chen, Mingzi; Jiang, Lihong; Li, Yue; Bai, Ge; Zhao, Jinghua; Zhang, Ming; Zhang, Jiantao

doi:10.18632/oncotarget.23498

Cited by 9 publications

(6 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As abdominal compartment syndrome leads to organ failure at an intra-abdominal pressure of 20 mmHg ( Hunter and Damani, 2004 ; Hedenstierna and Larsson, 2012 ), to assess the degree of severity that can be treated with this therapy, higher intra-abdominal pressures of 25, 30, 40, and 50 mmHg were also used. It was found that systemic and splanchnic blood flow and afferent hepatic flow were reduced as the intra-abdominal pressure rose; i.e., liver blood flow decreased by 39% when pneumoperitoneum increased from 10 to 15 mmHg and liver ischemic injury occurred ( Chen et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Stable Gastric Pentadecapeptide BPC 157 Therapy for Primary Abdominal Compartment Syndrome in Rats

et al. 2021

View full text Add to dashboard Cite

Recently, the stable gastric pentadecapeptide BPC 157 was shown to counteract major vessel occlusion syndromes, i.e., peripheral and/or central occlusion, while activating particular collateral pathways. We induced abdominal compartment syndrome (intra-abdominal pressure in thiopental-anesthetized rats at 25 mmHg (60 min), 30 mmHg (30 min), 40 mmHg (30 min), and 50 mmHg (15 min) and in esketamine-anesthetized rats (25 mmHg for 120 min)) as a model of multiple occlusion syndrome. By improving the function of the venous system with BPC 157, we reversed the chain of harmful events. Rats with intra-abdominal hypertension (grade III, grade IV) received BPC 157 (10 µg or 10 ng/kg sc) or saline (5 ml) after 10 min. BPC 157 administration recovered the azygos vein via the inferior–superior caval vein rescue pathway. Additionally, intracranial (superior sagittal sinus), portal, and caval hypertension and aortal hypotension were reduced, as were the grossly congested stomach and major hemorrhagic lesions, brain swelling, venous and arterial thrombosis, congested inferior caval and superior mesenteric veins, and collapsed azygos vein; thus, the failed collateral pathway was fully recovered. Severe ECG disturbances (i.e., severe bradycardia and ST-elevation until asystole) were also reversed. Microscopically, transmural hyperemia of the gastrointestinal tract, intestinal mucosa villi reduction, crypt reduction with focal denudation of superficial epithelia, and large bowel dilatation were all inhibited. In the liver, BPC 157 reduced congestion and severe sinusoid enlargement. In the lung, a normal presentation was observed, with no alveolar membrane focal thickening and no lung congestion or edema, and severe intra-alveolar hemorrhage was absent. Moreover, severe heart congestion, subendocardial infarction, renal hemorrhage, brain edema, hemorrhage, and neural damage were prevented. In conclusion, BPC 157 cured primary abdominal compartment syndrome.

show abstract

Section: Introductionmentioning

confidence: 99%

Stable Gastric Pentadecapeptide BPC 157 Therapy for Primary Abdominal Compartment Syndrome in Rats

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Moreover, the level of CC-16 increased to a greater degree in patients pretreated with morphine than in patients pretreated with hydromorphone ( Figure 6(a) ). As CO 2 pneumoperitoneum-induced lung injury is associated with systemic inflammatory and oxidative responses [ 34 ], we assessed the effects of hydromorphone on intercellular adhesion molecule-1 (ICAM-1) levels and the prooxidant-antioxidant balance (PAB), which has been shown to be closely related to inflammatory responses [ 35 , 36 ]. As shown in Figures 6(b) and 6(c) , ICAM-1 levels and the PAB in blood samples gradually increased with the duration of surgery in both groups.…”

Section: Resultsmentioning

confidence: 99%

Hydromorphone Protects against CO₂ Pneumoperitoneum‐Induced Lung Injury via Heme Oxygenase‐1‐Regulated Mitochondrial Dynamics

Shi

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Various pharmacological agents and protective methods have been shown to reverse pneumoperitoneum-related lung injury, but identifying the best strategy is challenging. Herein, we employed lung tissues and blood samples from C57BL/6 mice with pneumoperitoneum-induced lung injury and blood samples from patients who received laparoscopic gynecological surgery to investigate the therapeutic role of hydromorphone in pneumoperitoneum-induced lung injury along with the underlying mechanism. We found that pretreatment with hydromorphone alleviated lung injury in mice that underwent CO2 insufflation, decreased the levels of myeloperoxidase (MPO), total oxidant status (TOS), and oxidative stress index (OSI), and increased total antioxidant status (TAS). In addition, after pretreatment with hydromorphone, upregulated HO-1 protein expression, reduced mitochondrial DNA content, and improved mitochondrial morphology and dynamics were observed in mice subjected to pneumoperitoneum. Immunohistochemical staining also verified that hydromorphone could increase the expression of HO-1 in lung tissues in mice subjected to CO2 pneumoperitoneum. Notably, in mice treated with HO-1-siRNA, the protective effects of hydromorphone against pneumoperitoneum-induced lung injury were abolished, and hydromorphone did not have additional protective effects on mitochondria. Additionally, in clinical patients who received laparoscopic gynecological surgery, pretreatment with hydromorphone resulted in lower serum levels of club cell secretory protein-16 (CC-16) and intercellular adhesion molecule-1 (ICAM-1), a lower prooxidant-antioxidant balance (PAB), and higher heme oxygenase-1 (HO-1) activity than morphine pretreatment. Collectively, our results suggest that hydromorphone protects against CO2 pneumoperitoneum-induced lung injury via HO-1-regulated mitochondrial dynamics and may be a promising strategy to treat CO2 pneumoperitoneum-induced lung injury.

show abstract

“…Nrf2 plays a crucial role in cellular defenses against oxidative stress by regulating expression of antioxidant enzymes [38]. Normally, Keap1 binds Nrf2 to sequester it in the cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effects of Lactobacillus plantarum Strains on Non-Alcoholic Fatty Liver Disease in High Fat/High Fructose Diet-Fed Rats

et al. 2020

View full text Add to dashboard Cite

Emerging evidence suggests that probiotics are beneficial in non-alcoholic fatty liver disease (NAFLD). This study aimed to explore the effects of two Lactobacillus plantarum strains, ATG-K2 and ATG-K6 (isolated from Korean fermented cabbage), in a rat model of high fat/high fructose (HF/HF) diet-induced NAFLD. Rats with NAFLD were randomized into four groups (HF/HF diet control, (HC); HF/HF diet with silymarin, (PC); HF/HF diet with ATG-K2, (K2); and HF/HF diet with ATG-K6, (K6)) with healthy rats on a normal diet serving as the negative control. After treatment, histopathological and biochemical analyses of the blood and liver tissue were conducted. In addition, fecal microbiota was analyzed using the MiSeq platform. Compared with HC rats, K2 and K6 rats experienced significantly lower body weight gain, displayed decreased hepatic lipid accumulation, had lower serum levels of aspartate aminotransferase and alanine aminotransferase, and showed increased antioxidant enzyme activities. Moreover, de novo lipogenesis-related genes were downregulated following K2 and K6 administration. The fecal microbiota of K2 and K6 rats contained a higher proportion of Bacteriodetes and a lower proportion of Fimicutes than that of HC rats. Taken together, our results suggest that L. plantarum strains ATG-K2 and ATG-K6 are potential therapeutic agents for NAFLD.Nutrients 2020, 12, 542 2 of 16 of the transcription factors, such as sterol regulatory element binding protein 1c (SREBP-1c) and CCAAT/enhancer-binding protein alpha (C/EBPα), which in turn regulate the expression of hepatic gluconeogenesis and DNL genes [6]. It follows that fructose intake increases liver gluconeogenesis and DNL and elevates blood glucose and TG levels in humans [8,9] Another cause of NAFLD is oxidative stress. Fat deposition occurring in the liver results in lipid peroxidation, and it promotes a variety of responses such as inflammation and fibrosis. Thus, antioxidants (e.g., silymarin, vitamin E) are proposed as candidates for NAFLD treatment [10,11]; however, there are no standard pharmacological therapeutic agents for NAFLD yet. Recently, emerging evidence suggests that the gut-liver axis is strongly related to NAFLD. There are several reports published clinical trials applying probiotics on NAFLD patients [12]. Lactobacillus bulgaricus and Streptococcus thermophiles treatment improved liver aminotransferases levels in adult NAFLD patients [13]. In addition, probiotic capsules containing Lactobacillus acidophilus, Bifidobacterium lactis, Bifidobacterium bifidum, and Lactobacillus rhamnosus, as a supplement also decreased liver aminotransferases levels in obese children with NAFLD [14]. These results indicate that the intake of certain probiotics has a beneficial effect on NAFLD.Lactobacillus plantarum, which plays a key role in the production of various fermented foods, is one of the most important species of lactic acid bacteria (LAB). L. plantarum is found in diverse environments, such as the soil and the human gut, and is considered a potential pro...

show abstract

Hydrogen protects against liver injury during CO2 pneumoperitoneum in rats

Cited by 9 publications

References 71 publications

Stable Gastric Pentadecapeptide BPC 157 Therapy for Primary Abdominal Compartment Syndrome in Rats

Stable Gastric Pentadecapeptide BPC 157 Therapy for Primary Abdominal Compartment Syndrome in Rats

Hydromorphone Protects against CO₂ Pneumoperitoneum‐Induced Lung Injury via Heme Oxygenase‐1‐Regulated Mitochondrial Dynamics

Beneficial Effects of Lactobacillus plantarum Strains on Non-Alcoholic Fatty Liver Disease in High Fat/High Fructose Diet-Fed Rats

Contact Info

Product

Resources

About

Hydrogen protects against liver injury during CO2 pneumoperitoneum in rats

Cited by 9 publications

References 71 publications

Stable Gastric Pentadecapeptide BPC 157 Therapy for Primary Abdominal Compartment Syndrome in Rats

Stable Gastric Pentadecapeptide BPC 157 Therapy for Primary Abdominal Compartment Syndrome in Rats

Hydromorphone Protects against CO2 Pneumoperitoneum‐Induced Lung Injury via Heme Oxygenase‐1‐Regulated Mitochondrial Dynamics

Beneficial Effects of Lactobacillus plantarum Strains on Non-Alcoholic Fatty Liver Disease in High Fat/High Fructose Diet-Fed Rats

Contact Info

Product

Resources

About

Hydromorphone Protects against CO₂ Pneumoperitoneum‐Induced Lung Injury via Heme Oxygenase‐1‐Regulated Mitochondrial Dynamics