Modulatory activities of Chrysophyllum albidum and its fractions on microflora and colonic pump activities during inflammatory phase of colitis healing in experimental mice

Salami, Adeola Temitope; Odukanmi, Olugbenga Adeola; Oshode, Olubunmi Olamide; Olaleye, Samuel Babafemi

doi:10.1016/j.fbio.2017.12.015

Cited by 4 publications

(6 citation statements)

References 87 publications

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“…In this study also, there were notable increases in the protein concentrations of gastric tissue homogenate in the groups treated with C. albidum extracts. This observation further corroborates the protein anabolism activities of C. albidum and its chromatographic fractions as observed in earlier studies (Salami et al, 2018). C.albidum and its fractions ameliorated the exacerbated malondialdehyde (MDA) in gastric tissue to a minimal level though this reduction was more remarkable in HMeCaB.…”

Section: Discussionsupporting

confidence: 90%

“…This proton pump inhibiting activity of C.albidum might have been responsible for the low basal gastric output (BGO) and gastric acidity production observed in the previous study Salami and Famurewa, (2017). Earlier reports Salami et al, (2018) documented C.albidum to exert inhibitory H + K + ATPase activities as well as acting as a probiotic during the inflammatory phase of colitis healing. Previous studies reported that C.albidum contain flavonoids (earlier observed by Salami et al (2015) and its contained active phytochemical have been identified and isolated (Idowu et al, 2016) to be; procyanidin B5, epigallocatechin and epicatechin.…”

Section: Discussionmentioning

confidence: 99%

“…Delayed gastric ulcer healing activities of Chrysophyllum albidum has been documented (Salami and Famurewa, 2017) and was proposed to confer this activity through modulating inflammatory blood markers. Chrysophyllum albidum (G.Don) Sapotaceae family has been reported to have varied acclaimed medicinal properties: antinociceptive (Idowu et al, 2006), anti-colitis (Salami et al, 2018) and antihelmintic potentials (Salami et al, 2015). This probably is as a result of the inherent phytochemical constituents such as flavonoids, alkaloids, cardenolides, anthraquinones etc.…”

Section: Introductionmentioning

confidence: 99%

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Chrysophyllum Albidum Accelerates Delayed Gastric Ulcer Healing in Rats Through Oxidative Stress Reversal and Proton Pump Inhibition

Salami¹,

Famurewa²,

Omayone³

et al. 2021

njpr

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Background: Chrysophyllum albidum has been documented to exert its gastric ulcer (GU) healing activities by modulating blood inflammatory mediators, however, other probable in-vivo underlying mechanisms are still vague which this study sought to investigate.Materials and Methods: Male Wistar rats (120-130g) divided into 9 groups (n=15 for groups I-VII; n=5 for groups VIII & IX) viz: Groups I- positive control (DUnA); II and III–250 and 500mg/kg methanolic extract of C. albidum (MeCaB) bark respectively; IV, V and VI-100mg/kg fractions A, B and C respectively; VII–30mg/kg omeprazole; VIII-ulcerated untreated (baseline), IX-negative control. Chronic GU was induced experimentally and delayed using indomethacin with 14 days simultaneous drug treatment. Gastric ulcer score, mucin content, antioxidant and proton pump activities were evaluated by days 3, 7 and 14 of treatment. Data were expressed as Mean+SEM and P<0.05 was significant.Results: C. albidum and fractions treated groups significantly decreased gastric ulcer scores and lipid peroxidation compared with DUnA. Negative control, C. albidum and fraction treated groups significantly increased superoxide dismutase, catalase, glutathione levels and mucin content compared with DUnA group by days 3 and 7. C. albidum, Negative and baseline control groups significantly decreased H+K+ATPase activities compared with DUnA by day14.Conclusion: C. albidum and its fractions facilitated the healing of gastric ulcer, probably by enhanced antioxidant levels, mucin content and decreased gastric H+K+ATPase activity. Keywords: C. albidum and chromatographic fractions, gastric ulcer healing, mucin , antioxidant, H+/K+ATPase pump.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Chrysophyllum Albidum Accelerates Delayed Gastric Ulcer Healing in Rats Through Oxidative Stress Reversal and Proton Pump Inhibition

Salami¹,

Famurewa²,

Omayone³

et al. 2021

njpr

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“…A portion of stomach tissue was weighed and homogenized in phosphate buffer saline and centrifuged at 3,600 rpm for 15 min at 4°C to obtain a supernatant. The total protein content of gastric tissues was measured using the Biuret method (Gornall et al., 1949) with slight modification of infusing the Biuret reagent with potassium iodide, to prevent the precipitation of Cu 2+ as cuprous oxide as we have earlier reported (Salami et al, 2018). Malonaldehyde (MDA) levels were estimated colorimetrically as an indicator of lipid peroxidation (Adegoke et al., 2017; Buege and Steven, 1978), Catalase activity was measured as a function of the depletion of hydrogen peroxide (Aebi, 1984; Afolabi & Olagoke, 2020), Sulfhydryl content was assayed according to the method of Ellman, 1959 (Ellman, 1959), Nitric oxide was quantified indirectly as total nitrite (NO 2 − ) using Griess reagent (Ignarro et al., 1987; Salami et al., 2016) and the activity of sodium potassium pump in the gastric tissue was measured as phosphate release during incubation with Adenosine triphosphate (Bewaji et al., 1985; Salami, et al, 2018).…”

Section: Methodsmentioning

confidence: 99%

Potassium bromate cytotoxicity in the Wister rat model of chronic gastric ulcers: Possible reversal by protocatechuic acid

et al. 2020

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The affinity of xenobiotics for epithelial cells determine tissue and systemic toxicity expression. Humans come in contact with potassium bromate (KBrO 3 ; CAS. 7758-01-2) via exposure to mucus membrane and the skin when industrial workers inhale the white powdery substance or individuals use KBrO 3-containing cosmetics. (Alenius et al., 2014) Potassium bromate is also used as a food additive in baking, brewing, and cheese making (Emeje et al., 2010). Contact with KBrO 3 has been shown to predispose humans to central nervous system (CNS) perturbations like impaired thought pattern, deafness, and spasms, as well as systemic pathologies like renal malfunction, hypotension, cyanosis, methemoglobinemia, and cardiac arrhythmia

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“…Our previous study showed that silencing ATP4a not only inhibited H+/K+ transport, but also increased intracellular glycolysis (12). Additionally, the expression of ATP4a, which is closely related to the severity of colitis, was decreased (13,14). In this study, we also found that glycolysis in cmECs was significantly increased, the expression of pyruvate dehydrogenase kinase 4 (PDK) protein was upregulated, and the expression of ATP4a was downregulated in colitis.…”

Section: Introductionmentioning

confidence: 99%

Panax notoginseng attenuates hypoxia-induced glycolysis in colonic mucosal epithelial cells in DSS-induced colitis

He¹,

Pan²,

Peng³

et al. 2022

Ann Transl Med

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Background: Colonic mucosal injuries are an important manifestation of ulcerative colitis (UC), which is related to hypoxia-induced glycolysis in colonic mucosal epithelial cells (cmECs). Panax notoginseng (PN) promotes the repair of colonic mucosal injuries by inhibiting hypoxia-induced glycolysis in cmECs; However, the mechanism by which this occurs is not completely clear. Here, we are to investigate the effects of PN on glucose metabolism in cmECs in colitis and the underlying mechanism.Methods: A model of dextran sulfate sodium-induced colitis rats was used in this research, and the severity of colitis was assessed by pathology, disease activity index (DAI), and weight changes. The content of intracellular pyruvate, intracellular lactate, adenosine triphosphate (ATP), reactive oxygen species (ROS), mitochondrial ROS (mtROS), myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity, and inflammatory cytokines was detected by assay kits. The expression levels of proteins were detected by western blotting. The expression levels of the ATP4a gene were detected by quantitative polymerase chain reaction (QT-PCR). Results:The colonic mucosal injuries of the colitis rats were significantly worse than those of the control group. Specifically, the hypoxia-induced glycolysis and potential of hydrogen (pH) in the colonic lumen were increased, and the expression of ATP4a was downregulated in the colitis rats. PN (1.0 g/kg) promoted the repair of colonic mucosal injuries, and reversed the pH in the colonic lumen. Further, PN increased the expression of ATP4a proteins, the content of ATP, and the SOD activity, and decreased the expression of pyruvate dehydrogenase lipoamide kinase isozyme and hypoxia-inducible factor 1-alpha proteins, the content of ROS, and MPO activity in cmECs in colitis. PN also increased the expression of ATP4a, cytochrome P450 family 21 subfamily a member 2, and hydroxy-delta-5-steroid dehydrogenase, 3 beta and steroid deltaisomerase 2 proteins in the mitochondria, and decreased the content of mtROS in cmECs.Conclusions: PN alleviated the pH in the colonic lumen and hypoxia-induced glycolysis in cmECs by reducing the hypoxia-induced glycolysis caused by the downregulation of ATP4a protein, thereby promoting the repair of colonic mucosal injuries in colitis.

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Modulatory activities of Chrysophyllum albidum and its fractions on microflora and colonic pump activities during inflammatory phase of colitis healing in experimental mice

Cited by 4 publications

References 87 publications

Chrysophyllum Albidum Accelerates Delayed Gastric Ulcer Healing in Rats Through Oxidative Stress Reversal and Proton Pump Inhibition

Chrysophyllum Albidum Accelerates Delayed Gastric Ulcer Healing in Rats Through Oxidative Stress Reversal and Proton Pump Inhibition

Potassium bromate cytotoxicity in the Wister rat model of chronic gastric ulcers: Possible reversal by protocatechuic acid

Panax notoginseng attenuates hypoxia-induced glycolysis in colonic mucosal epithelial cells in DSS-induced colitis

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