Sepsis and septic shock are still a leading cause of mortality and morbidity in intensive care units worldwide. Sepsis is an uncontrolled and excessive response of the innate immune system toward the invading infectious microbes, characterized by the hyper‐production of pro‐inflammatory mediators such as interleukin (IL)‐1β, IL‐6, tumor‐necrosis factor (TNF)‐α, and high‐mobility group box 1 (HMGB1). In severe sepsis, the overwhelming production of pro‐inflammatory cytokines and reactive oxygen species may compromise organ function and lead to the induction of abnormal apoptosis in different organs, resulting in multiple organ dysfunction syndrome and death. Hence, compounds that are able to attenuate inflammatory responses may have therapeutic potential for sepsis treatment. Understanding the pathophysiology and underlying molecular mechanisms of sepsis may provide useful insights in the discovery and development of new effective therapeutics. Therefore, numerous studies have invested much effort into elucidating the mechanisms involved with the onset and development of sepsis. The present review mainly focuses on the molecules and signaling pathways involved in the pathogenicity of sepsis. Additionally, several well‐known natural bioactive herbal compounds and phytochemicals, which have shown protective and therapeutic effects with regard to sepsis, as well as their mechanisms of action, are presented. This review suggests that these phytochemicals are able to attenuate the overwhelming inflammatory responses developed during sepsis by modulating different signaling pathways. Moreover, the anti‐inflammatory and cytoprotective activities of phytochemicals make them potent compounds to be included as complementary therapeutic agents in the diets of patients suffering from sepsis in an effort to alleviate sepsis and its life‐threatening complications, such as multi‐organ failure.

Traumatic brain injury (TBI) is one of the most prevalent causes of permanent physical and cognitive disabilities. TBI pathology results from primary insults and a multi-mechanistic biochemical process, termed as secondary brain injury. Currently, there are no pharmacological agents for definitive treatment of patients with TBI. This article is presented with the purpose of reviewing molecular mechanisms of TBI pathology, as well as potential strategies and agents against pathological pathways. In this review article, materials were obtained by searching PubMed, Scopus, Elsevier, Web of Science, and Google Scholar. This search was considered without time limitation. Evidence indicates that oxidative stress and mitochondrial dysfunction are two key mediators of the secondary injury cascade in TBI pathology. TBI-induced oxidative damage results in the structural and functional impairments of cellular and subcellular components, such as mitochondria. Impairments of mitochondrial electron transfer chain and mitochondrial membrane potential result in a vicious cycle of free radical formation and cell apoptosis. The results of some preclinical and clinical studies, evaluating mitochondria-targeted therapies, such as mitochondriatargeted antioxidants and compounds with pleiotropic effects after TBI, are promising. As a proposed strategy in recent years, mitochondria-targeted multipotential therapy is a new hope, waiting to be confirmed. Moreover, based on the available findings, biologics, such as stem cell-based therapy and transplantation of mitochondria are novel potential strategies for the

Background Nutritional status of patients with COVID‐19 can affect the recovery process of patients; however, no nutritional scale was introduced to evaluate the nutritional status of the patients. Thus, the main objective of this study was to examine the usefulness of Nutritional status‐2002 (NRS‐2002) among COVID‐19 patients admitted to the intensive care unit (ICU). Material and Methods In this cross‐sectional study, 73 patients with definitive corona diagnosis admitted to the ICUs of Al‐Zahra hospital, Isfahan, Iran in October 2020 to January 2021 were recruited. Dietary intake, NRS‐2002, demographic, anthropometric and biochemical indices of patients were recorded. Results The majority of patients were at risk for moderate (69.9%) to severe (12.3%) malnutrition. Daily calorie intake ( P = .001) and albumin ( P = .001) levels in deceased patients were significantly lower than the recovered group. A direct correlation between NRS‐2002 and age ( P < .001) and an inverse correlation with daily calorie intake ( P = .002), albumin ( P = .05) and PaO2 ( P = .034) was found. Moreover, there is a strong correlation between NRS‐2002 score and chance of death among COVID‐19 patients (OR=34.5, 95%CI:(5.2 ‐ 228.93), P‐value<0.001). Likewise, the levels of bilirubin direct (OR=8, 95%CI:(1.30 ‐ 49.38), P‐value=0.025) and creatine‐phosphokinase (OR=0.9, 95%CI:(0.99 ‐ 1.00), P‐value=0.035) have a significant direct association with chance of death. Conclusion Results showed patients with COVID‐19 admitted to the ICU did not have appropriate nutritional status and mortality was higher among patients with lower amounts of the serum albumin and daily calorie intakes. Furthermore, there is a strong association between the NRS‐2002 index and the chance of mortality in these patients.

Neuroprotective effects of curcumin have been shown in previous studies. This updated systematic review of clinical trials aimed to investigate the effect of curcumin on neurological disorders. Databases including PubMed, Scopus, Web of Science, and Google Scholar were systematically searched to identify clinical trials investigating the effects of curcumin/turmeric supplements alone, or in combination with other ingredients, on neurological diseases. Nineteen studies comprising 1,130 patients met the inclusion criteria. Generally, intervention and study outcomes were heterogeneous. In most of the studies, curcumin had a favorable effect on oxidative stress and inflammation. However, with the exception of AD, curcumin supplementation either alone, or in combination with other ingredients, had beneficial effects on clinical outcomes for the other aforementioned neurodegenerative diseases. For example, the frequency, severity, and duration of migraine attacks, scores on the revised ALS functional rating scale, and the occurrence of motor complications in PD were all significantly improved with curcumin supplementation either alone or in combination with other ingredients. However, in three studies, several adverse side effects (mostly gastrointestinal in nature) were reported. Curcumin supplementation may have favorable effects on inflammatory status and clinical outcomes of patients with neurological disease, although the results were not consistent.