Spirina Liudmila V, Masunov Vladimir N, Dyakov Denis A, Akbasheva Olga E, Kebekbayeva Amina Y, Shuvalov Igor Yu, Masunova Nadezhda V, Kovaleva Irina V, Dagbaeva Yumzhana
Siberian State Medical University, Tomsk, Russia.
Cancer Research Institute, Tomsk National Research Medical Center, Tomsk, Russia.
Indian J Clin Biochem. 2022 Nov 12;38(4):1-10. doi: 10.1007/s12291-022-01089-x.
Multiple pathogenic mechanisms are found in SARS-CoV2 systemic inflammation. Oxidative stress, altered proteolysis, hypercoagulation, and metabolic disorders are significant in virus-induced lesions. The study aimed to investigate the biochemical mechanism of virus-induced disorders and determine the biochemical features in SARS-CoV2-associated liver damage and intestine lesions. A retrospective case series of ninety-two patients diagnosed with COVID-19 pnemonia. The ACE, α1-proteinase inhibitor, trypsin-like proteinase, and elastase activity were measured. Nitrites level was detected in reaction with Griess reagent. The ELISA kit measured Troponin, C-peptide, leptin, adiponectin, PAR4, and neuropilin level. It was obtained an increase in ACE activity and nitrites ions content in SARS-CoV2 associated patients. The hyperglycemia and an increase in adipose tissue-derived hormones guided the virus-induced metabolic disorders. Proteolysis activation was revealed in SARS-CoV2 pneumonia patients. The found molecular event was accompanied by hyperglycemia induction. Multiorgan lesions manifest in in cardiac failure, which was detected in patients with ARDS. Moreover, high arterial blood pressure in patients with COVID-19 was associated with the hyperglycemia and increased ACE activity and NO ions level. Liver damage was specific for COVID-19-associated patients with severe ARDS and heart failure. Proteolysis overactivation resulting in vasoactive substances imbalance was detected in patients with the intestinal lesions. The obtained data shows the the neuropilin-dependent axis in damage prevalence in the intestine. Metabolic disorders resulting in the growth of adipose-derived tissue hormones, nitrites, and neuropilin levels was triggered by prolonged inflammation. So, the impaired metabolism and SARS-CoV2 associated hyperglycemia influence on SARS-CoV2 multiple mechanisms. Gastrointestinal manifestations in SARS-CoV2 infection was found to be related to various biochemical and molecular tools. ACE2 receptors axis is prevalent for liver damage, but NRP-1 protein (neuropilin), NO derivatives, and adipose tissue-derived hormones are essential for intestinal lesions.
The online version contains supplementary material available at 10.1007/s12291-022-01089-x.
在新型冠状病毒2型（SARS-CoV2）引起的全身炎症中发现了多种致病机制。氧化应激、蛋白水解改变、高凝状态和代谢紊乱在病毒诱导的损伤中具有重要意义。本研究旨在探讨病毒诱导紊乱的生化机制，并确定SARS-CoV2相关肝损伤和肠道病变的生化特征。一项对92例诊断为新冠肺炎肺炎患者的回顾性病例系列研究。检测了血管紧张素转换酶（ACE）、α1-蛋白酶抑制剂、胰蛋白酶样蛋白酶和弹性蛋白酶活性。用格里斯试剂检测亚硝酸盐水平。采用酶联免疫吸附测定（ELISA）试剂盒检测肌钙蛋白、C肽、瘦素、脂联素、蛋白酶激活受体4（PAR4）和神经纤毛蛋白水平。结果发现，SARS-CoV2相关患者的ACE活性和亚硝酸盐离子含量增加。高血糖和脂肪组织衍生激素的增加导致了病毒诱导的代谢紊乱。在SARS-CoV2肺炎患者中发现了蛋白水解激活。所发现的分子事件伴随着高血糖的诱导。多器官损伤表现为心力衰竭，在急性呼吸窘迫综合征（ARDS）患者中检测到。此外，新冠肺炎患者的高血压与高血糖、ACE活性增加和一氧化氮（NO）离子水平升高有关。肝损伤是SARS-CoV2相关严重ARDS和心力衰竭患者的特异性表现。在肠道病变患者中检测到蛋白水解过度激活导致血管活性物质失衡。获得的数据显示了神经纤毛蛋白依赖性轴在肠道损伤发生率中的作用。长期炎症引发了代谢紊乱，导致脂肪组织衍生激素、亚硝酸盐和神经纤毛蛋白水平升高。因此，代谢受损和SARS-CoV2相关的高血糖影响SARS-CoV2的多种机制。发现SARS-CoV2感染中的胃肠道表现与各种生化和分子工具有关。ACE2受体轴在肝损伤中普遍存在，但神经纤毛蛋白-1（NRP-1）蛋白（神经纤毛蛋白）、NO衍生物和脂肪组织衍生激素对肠道病变至关重要。
在线版本包含可在10.1007/s12291-022-01089-x获取的补充材料。
