Myoelectric activity and motility of the Roux limb after cut or uncut Roux-en-Y gastrojejunostomy

AIM: To explore the mechanisms of uncut Roux-en-Y gastrojejunostomy, which is used to decrease the occurrence of Roux stasis syndrome.METHODS: The changes of myoelectric activity, mechanic motility and interstitial cells of Cajal (ICC) of the Roux limb after cut or uncut Roux-en-Y gastrojejunostomy were observed. RESULTS: When compared with the cut group, the amplitude (1.15 ± 0.15 mV vs 0.48 ± 0.06 mV, P < 0.05) and frequency (14.4 ± 1.9 cpm vs 9.5 ± 1.1 cpm, P < 0.01) of slow waves and the incidence (98.2% ± 10.4% vs 56.6% ± 6.4%, P < 0.05) and amplitude (0.58 ± 0.08 mV vs 0.23 ± 0.06 mV, P < 0.01) of spike potential of the Roux limb in the uncut group were significantly higher. The migrating myoelectric complexes (MMC) phase Ⅲ duration in the uncut group was significantly prolonged (6.5 ± 1.1 min vs 4.4 ± 0.8 min, P < 0.05), while the MMC cycle obviously shortened (42.5 ± 6.8 vs 55.3 ± 8.2 min, P < 0.05). Both gastric emptying rate (65.5% ± 7.9% vs 49.3% ± 6.8%, P < 0.01) and intestinal impelling ratio (53.4% ± 7.4% vs 32.2% ± 5.4%, P < 0.01) in the uncut group were significantly increased. The contractile force index of the isolated jejunal segment in the uncut group was significantly higher (36.8 ± 5.1 vs 15.3 ± 2.2, P < 0.01), and the expression of c-kit mRNA was significantly increased in the uncut group (0.82 ± 0.11 vs 0.35 ± 0.06, P < 0.01). CONCLUSION: Uncut Roux-en-Y gastrojejunostomymay lessen the effects of operation on myoelectric activity such as slow waves, spike potential, and MMC, decrease the impairment of gastrointestinal motility, and remarkably increase the expression of c-kit mRNA.

Withaferin A inhibits ferroptosis and protects against intracerebral hemorrhage

Recent studies have indicated that suppressing oxidative stress and ferroptosis can considerably improve the prognosis of intracerebral hemorrhage(ICH).Withaferin A(WFA),a natural compound,exhibits a positive effect on a number of neurological diseases.However,the effects of WFA on oxidative stress and ferroptosis-mediated signaling pathways to ICH remain unknown.In this study,we investigated the neuroprotective effects and underlying mechanism for WFA in the regulation of ICH-induced oxidative stress and ferroptosis.We established a mouse model of ICH by injection of autologous tail artery blood into the caudate nucleus and an in vitro cell model of hemin-induced ICH.WFA was injected intracerebroventricularly at 0.1,1 or 5μg/kg once daily for 7 days,starting immediately after ICH operation.WFA markedly reduced brain tissue injury and iron deposition and improved neurological function in a dose-dependent manner 7 days after cerebral hemorrhage.Through in vitro experiments,cell viability test showed that WFA protected SH-SY5Y neuronal cells against hemin-induced cell injury.Enzyme-linked immunosorbent assays in vitro and in vivo showed that WFA markedly decreased the level of malondialdehyde,an oxidative stress marker,and increased the activities of anti-oxidative stress markers superoxide dismutase and glutathione peroxidase after ICH.Western blot assay,quantitative polymerase chain reaction and immunofluorescence results demonstrated that WFA activated the nuclear factor E2-related factor 2(Nrf2)/heme oxygenase-1(HO-1)signaling axis,promoted translocation of Nrf2 from the cytoplasm to nucleus,and increased HO-1 expression.Silencing Nrf2 with siRNA completely reversed HO-1 expression,oxidative stress and protective effects of WFA.Furthermore,WFA reduced hemin-induced ferroptosis.However,after treatment with an HO-1 inhibitor,the neuroprotective effects of WFA against hemin-induced ferroptosis were weakened.MTT test results showed that WFA combined with ferrostatin-1 reduced hemin-induced SH-SY5Y neuronal cell injury.Our findings reveal that WFA treatment alleviated ICH injury-induced ferroptosis and oxidative stress through activating the Nrf2/HO-1 pathway,which may highlight a potential role of WFA for the treatment of ICH.