The effects of quercetin on liver regeneration after liver resection in rats

Mandic, P; Leštarević, S.; Filipović, Tatjana; Savic, Sladjana; Stević, S.; Kostić, Milan

doi:10.5603/fm.a2015.0097

Cited by 6 publications

(11 citation statements)

References 36 publications

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“…The regenerative process following liver resection may trigger apoptotic pathways, resulting in the activation of apoptotic cells 40 . In addition, the surgical trauma itself can cause oxidative stress and inflammation, which may contribute to cell death and apoptosis 41 , 42 . The previous study showed that apoptotic liver cells were significantly increased in the liver resection group compared with the sham group 43 .…”

Section: Discussionmentioning

confidence: 99%

CBX7 silencing promoted liver regeneration by interacting with BMI1 and activating the Nrf2/ARE signaling pathway

Dou,

Lu,

et al. 2024

Sci Rep

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Multiple studies have shown knockdown of chromobox 7 (CBX7) promotes the regenerative capacity of various cells or tissues. We examined the effect of CBX7 on hepatocyte proliferation and liver regeneration after 2/3 hepatectomy in a mouse model. For in vitro experiments, NCTC 1469 and BNL CL.2 hepatocytes were co-transfected with siRNA-CBX7-1 (si-CBX7-1), siRNA-CBX7-2 (si-CBX7-2), pcDNA-CBX7, si-BMI1-1, si-BMI1-2, pcDNA-BMI1, or their negative control. For in vivo experiments, mice were injected intraperitoneally with lentivirus-packaged shRNA and shRNA CBX7 before hepatectomy. Our results showed that CBX7 was rapidly induced in the early stage of liver regeneration. CBX7 regulated hepatocyte proliferation, cell cycle, and apoptosis of NCTC 1469 and BNL CL.2 hepatocytes. CBX7 interacted with BMI1 and inhibited BMI1 expression in hepatocytes. Silencing BMI1 aggregated the inhibitory effect of CBX7 overexpression on hepatocyte viability and the promotion of apoptosis. Furthermore, silencing BMI1 enhanced the regulatory effect of CBX7 on Nrf2/ARE signaling in HGF-induced hepatocytes. In vivo, CBX7 silencing enhanced liver/body weight ratio in PH mice. CBX7 silencing promoted the Ki67-positive cell count and decreased the Tunel-positive cell count after hepatectomy, and also increased the expression of nuclear Nrf2, HO-1, and NQO-1. Our results suggest that CBX7 silencing may increase survival following hepatectomy by promoting liver regeneration.

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Section: Discussionmentioning

confidence: 99%

CBX7 silencing promoted liver regeneration by interacting with BMI1 and activating the Nrf2/ARE signaling pathway

Dou,

Lu,

et al. 2024

Sci Rep

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“…[18][19][20][21] Delayed colonic transit was associated with reduced glial Ca 2+ responses and changes in connexin-43, a member of gap junction proteins, in middle-aged (12 months old) mice. 22 Although reduced enteric glia is also observed in humans, 23,24 detailed mechanisms…”

Section: Overvie W Of the Cellul Ar And Fun C Tional Chang E S With Ag Ementioning

confidence: 99%

“…Delayed colonic transit was associated with reduced glial Ca 2+ responses and changes in connexin‐43, a member of gap junction proteins, in middle‐aged (12 months old) mice 22 . Although reduced enteric glia is also observed in humans, 23,24 detailed mechanisms remain unclear. Surprisingly, a recent report suggests that a subpopulation of enteric neurons, but not glia, originate from mesoderm and during aging these mesoderm‐derived neurons become dominant form of all neurons in the enteric nervous system 25 .…”

Section: Overview Of the Cellular And Functional Changes With Agementioning

confidence: 99%

Aging of enteric neuromuscular systems in gastrointestinal tract

Nguyen

Taheri

Chandra

et al. 2022

Neurogastroenterology Motil

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Background Aging is a complex biological process and associated with a progressive decline in functions of most organs including the gastrointestinal (GI) tract. Age‐related GI motor disorders/dysfunctions include esophageal reflux, dysphagia, constipation, fecal incontinence, reduced compliance, and accommodation. Although the incidence and severity of these diseases and conditions increase with age, they are often underestimated due in part to nonspecific and variable symptoms and lack of sufficient medical attention. They negatively affect quality of life and predispose the elderly to other diseases, sarcopenia, and frailty. The mechanisms underlying aging‐associated GI dysfunctions remain unclear, and there is limited data examining the effect of aging on GI motor functions. Many studies on aging‐associated changes to cells within the tunica muscularis including enteric neurons, smooth muscles, and interstitial cells have proposed that cell loss and/or molecular changes may be involved in the pathogenesis of age‐related GI motor disorders/dysfunctions. There is also evidence that the aging contributes to phenotypic changes in innate immune cells, which are physically and functionally linked to other cells in the tunica muscularis and can alter GI (patho) physiology. However, various patterns of changes have been reported, some of which are contradictory, indicating a need for additional work in this area. Purpose Although GI infection due to intestinal bacterial overgrowth, bleeding, and cancers are also important and common problems in the elderly patients, this mini‐review focuses on data obtained from enteric neuromuscular aging research with the goal of better understanding the cellular and molecular mechanisms of enteric neuromuscular aging to enhance future therapy.

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“…The ageing of the gastrointestinal tract has been studied by many authors and their studies have demonstrated various changes related to its function and morphology. Prior studies have pointed to a significant decrease in myenteric neurons at the level of the esophagus and small and large intestines [5,6]. Some of them have reported that the loss of the neurons in older individuals could be compensated by a corresponding enlargement of the neuronal perikarya and their nuclei [5].…”

mentioning

confidence: 99%

“…Prior studies have pointed to a significant decrease in myenteric neurons at the level of the esophagus and small and large intestines [5,6]. Some of them have reported that the loss of the neurons in older individuals could be compensated by a corresponding enlargement of the neuronal perikarya and their nuclei [5]. Other research has shown a decrease in the overall number of neurons per square cm.…”

mentioning

confidence: 99%

Morphometric Changes of the Myenteric Plexus in the Colon of the Mice-D-Galactose Ageing Model

Genov,

Tomov,

Dimitrov

et al. 2024

C. R. Acad. Bulg. Sci.

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Ageing-related diseases are paramount for understanding the socioeconomic impact of the postmodern society. Neuronal degeneration is a known phenomenon in ageing. The D-galactose model of accelerated ageing is widely used in age-associated neuronal cell death because of the oxidative stress it induces, which correlates to reduced cognitive performance and robustly detectable neuronal shrinkage in the CNS. This study aims at demonstrating the morphological changes of neurons of the myenteric plexus in mice treated with D-galactose. D-galactose was given orally with drinking water, resulting in an average dose of 500 mg/kg daily for six weeks. In the D-galactose accelerated ageing model, a significant size reduction of the neuronal perikarya of the myenteric plexus was observed all along the large intestine. The average soma area at the caecum in the control group was 305 µm2, which was reduced by almost 20% in the ageing model. In contrast, at the level of the proximal colon in the D-galactose ageing model, the average area of the neuronal soma was 280 µm2, a reduction of 30%. The most significant reduction has been observed at the level of the distal colon, where the neuronal soma was reduced by 40%. There is a significant reduction of the area of the neuronal bodies in the myenteric plexus among different parts of the mice's large intestine in the accelerated ageing model. It can be inferred that D-galactose-induced morphological changes in the myenteric plexus may be related to the increased gastrointestinal motility dysfunction with ageing.

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The effects of quercetin on liver regeneration after liver resection in rats

Abstract: (Folia Morphol 2016; 75, 2: 188-195)

Cited by 6 publications

References 36 publications

CBX7 silencing promoted liver regeneration by interacting with BMI1 and activating the Nrf2/ARE signaling pathway

CBX7 silencing promoted liver regeneration by interacting with BMI1 and activating the Nrf2/ARE signaling pathway

Aging of enteric neuromuscular systems in gastrointestinal tract

Morphometric Changes of the Myenteric Plexus in the Colon of the Mice-D-Galactose Ageing Model

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