Chronic liver disease (CLD) is a continuous process that causes a reduction of liver function lasting more than six months. CLD includes alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), chronic viral infection, and autoimmune hepatitis, which can lead to liver fibrosis, cirrhosis, and cancer. Liver inflammation and oxidative stress are commonly associated with the development and progression of CLD. Molecular signaling pathways such as AMP-activated protein kinase (AMPK), C-Jun N-terminal kinase, and peroxisome proliferator-activated receptors (PPARs) are implicated in the pathogenesis of CLD. Therefore, antioxidant and anti-inflammatory agents from natural products are new potent therapies for ALD, NAFLD, and hepatocellular carcinoma (HCC). In this review, we summarize some powerful products that can be potential applied in all the stages of CLD, from ALD/NAFLD to HCC. The selected agents such as β-sitosterol, curcumin, genistein, and silymarin can regulate the activation of several important molecules, including AMPK, Farnesoid X receptor, nuclear factor erythroid 2-related factor-2, PPARs, phosphatidylinositol-3-kinase, and lysyl oxidase-like proteins. In addition, clinical trials are undergoing to evaluate their efficacy and safety.

Antioxidant and anti-inflammatory agents in chronic liver diseases: Molecular mechanisms and therapy

Liver fibrosis accompanies the progression of chronic liver diseases independent of etiologies, such as hepatitis viral infection, alcohol consumption, and metabolic-associated fatty liver disease. It is commonly associated with liver injury, inflammation, and cell death. Liver fibrosis is characterized by abnormal accumulation of extracellular matrix components that are expressed by liver myofibroblasts such as collagens and alpha-smooth actin proteins. Activated hepatic stellate cells contribute to the major population of myofibroblasts. Many treatments for liver fibrosis have been investigated in clinical trials, including dietary supplementation (e.g., vitamin C), biological treatment (e.g., simtuzumab), drug (e.g., pegbelfermin and natural herbs), genetic regulation (e.g., non-coding RNAs), and transplantation of stem cells (e.g., hematopoietic stem cells). However, none of these treatments has been approved by Food and Drug Administration. The treatment efficacy can be evaluated by histological staining methods, imaging methods, and serum biomarkers, as well as fibrosis scoring systems, such as fibrosis-4 index, aspartate aminotransferase to platelet ratio, and non-alcoholic fatty liver disease fibrosis score. Furthermore, the reverse of liver fibrosis is slowly and frequently impossible for advanced fibrosis or cirrhosis. To avoid the life-threatening stage of liver fibrosis, anti-fibrotic treatments, especially for combined behavior prevention, biological treatment, drugs or herb medicines, and dietary regulation are needed. This review summarizes the past studies and current and future treatments for liver fibrosis.

Treatment of liver fibrosis: Past, current, and future

Excess free iron is a substrate for the formation of reactive oxygen species (ROS), thereby augmenting oxidative stress. Oxidative stress is a well-established cause of organ damage in the liver, the main site of iron storage. Ferroptosis, an iron-dependent mechanism of regulated cell death, has recently been gaining attention in the development of organ damage and the progression of liver disease. We therefore summarize the main mechanisms of iron metabolism, its close connection to oxidative stress and ferroptosis, and its particular relevance to disease mechanisms in metabolic-dysfunction-associated fatty liver disease and potential targets for therapy from a clinical perspective.

Iron, Oxidative Stress, and Metabolic Dysfunction—Associated Steatotic Liver Disease

Autophagy is an evolutionarily conserved eukaryotic intracellular degradation process. Although the molecular mechanisms of plant autophagy share similarities with those in yeast and mammals, certain unique mechanisms have been identified. Recent studies have highlighted the importance of autophagy during vegetative growth stages as well as in plant-specific developmental processes, such as seed development, germination, flowering, and somatic reprogramming. Autophagy enables plants to adapt to and manage severe environmental conditions, such as nutrient starvation, high-intensity light stress and heat stress, leading to intracellular remodeling and physiological changes in response to stress. In the past, plant autophagy research lagged behind similar studies in yeast and mammals; however, recent advances have greatly expanded our understanding of plant-specific autophagy mechanisms and functions. This review summarizes the current state of knowledge and latest research findings on the mechanisms and roles of plant autophagy with the objective of improving our understanding of this vital process in plants.

New Insights into Plant Autophagy: Molecular Mechanisms and Roles in Development and Stress Responses.

Traumatic brain injury (TBI) is an important cause of disability and death. TBI leads to multiple forms of nerve cell death including ferroptosis due to iron-dependent lipid peroxidation. Anacardic acid (AA) is a natural component extracted from cashew nut shells, which has been reported to have neuroprotective effects in traumatic brain injury. We investigated whether AA has an anti-ferroptosis effect in TBI.We used the Feeney free-fall impact method to construct a TBI model to investigate the effect of AA on ferroptosis caused by TBI, in which Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, served as a positive control group. We first identified the therapeutic effect of AA on TBI through modified neurological severity score (mNSS) and determined the appropriate concentration. Secondly, we investigated the effect of AA on the expression level of the key protein of ferroptosis by Western blotting and immunohistochemistry. Then the effect of AA on nerve tissue injury and nerve function improvement was verified. Finally, enzym-linked immunosorbent assay (ELISA) was used to verify that AA could reduce inflammation after TBI.We found the intensely inhibitory effect of AA on ferroptosis, which is in parallel with the results obtained after Fer-1 treatment. In addition, AA and Fer-1 mitigated TBI-mediated tissue defects, destruction of the blood-brain barrier, and neurodegeneration. Novel object recognition (NOR), mNSS and water maze test showed that AA could significantly reduce the impairment of neural function and behavioral cognitive ability caused by TBI. Finally, we also demonstrated that AA has not only an anti-ferroptosis effect, but also an anti-inflammation effect.AA can reduce the neurological impairment and behavioral cognitive impairment caused by TBI through the dual effect of anti-ferroptosis and anti-inflammation. 

Anacardic acid improves neurological deficits in traumatic brain injury by anti-ferroptosis and anti-inflammation

Autophagy functions in plant host immunity responses to pathogen infection. The molecular mechanisms and functions used by the citrus Huanglongbing (HLB)-associated intracellular bacterium 'Candidatus Liberibacter asiaticus' (CLas) to manipulate autophagy are unknown. We identified a CLas effector, SDE4405 (CLIBASIA_04405), which contributes to HLB progression. Transgenic SDE4405 in Wanjincheng orange (Citrus sinensis) promotes CLas proliferation and symptom expression via suppressing host immunity response. SDE4405 interacts with ATG8-family proteins (ATG8s) and their interactions activate autophagy in Nicotiana benthamiana. The occurrence of autophagy is also significantly enhanced in SDE4405-transgenic citrus plants. Interrupting NbATG8s-SDE4405 interaction by silencing NbATG8s reduces Pseudomonas syringae pv. tomato strain DC3000ΔhopQ1-1 (Pst DC3000ΔhopQ1-1) proliferation in N. benthamiana, and transient overexpression of CsATG8c and SDE4405 in citrus promotes Xanthomonas citri subsp. citri (Xcc) multiplication, suggesting SDE4405-ATG8s interaction negatively regulates plant defense. These data show the role of the CLas effector protein in manipulating autophagy and provide new insights into the molecular interaction between CLas and citrus.

An effector of 'Candidatus Liberibacter asiaticus' manipulates autophagy to promote bacterial infection.

To explore the effect of curcumol on autophagy and ferroptosis of hepatic stellate cells, and to clarify the molecular mechanism of its anti‐hepatic fibrosis. In the present study, we report that curcumol promotes the death of activated HSCs and reduces the deposition of extracellular matrix. Interestingly, curcumol treatment can trigger ferroptosis to eliminate activated HSCs characterized by iron overload, lipid ROS accumulation, glutathione depletion, and lipid peroxidation. Curcumol promotes HSC autophagy, which may be the key mechanism for its induction of ferroptosis. It is worth noting that the upregulation of nuclear receptor coactivator 4 (NCOA4) may play a key molecular mechanism. NCOA4 mediates the release of iron ions and induces the occurrence of ferroptosis. Overall, curcumol promotes autophagy in hepatic stellate cells, mediates the degradation of NCOA4 and FTH1 complexes, releases iron ions, leads to iron overload, and induces ferroptosis, which may be an important mechanism for its anti‐hepatic fibrosis effect.

Curcumol alleviates liver fibrosis through inducing autophagy and ferroptosis in hepatic stellate cells

Object: The use of traditional Ghinese Medicine Inheritance assistance system (TMC) for the treatment of chronic atrophic gastritis prescription and the rule of compatibility. Methods: Computer - based Retrieval of Chinese journal full-text database (CNKI) for the treatment of chronic atrophic gastritis related literature, search time limit: 2008-2018. In order to explore the combination of high frequency drug pairs and new prescriptions, the database was established with the aid of traditional Chinese medicine inheritance system. The purpose of this paper was to demonstrate the clinical experience of traditional Chinese medicine in the past ten years, and to find a new breakthrough for the treatment of CAG in traditional Chinese medicine. Result: After screening 223 prescriptions that met the inclusion criteria, including 217 herbs of traditional Chinese medicine, the statistical results show that in the treatment of CAG, the main medicine is invigorating qi and invigorating spleen and Codonopsis and Atractylodes macrocephala are the most common. Combined rule analysis showed that Atractylodes macrocephala had the most association with other drugs. The six new formulas are summarized again. Conclusion: Through the data mining statistical analysis, the prescription of treating CAG included in the selected database is mainly invigorating spleen and stomach, regulating qi, warming and tonifying deficiency, activating blood circulation, nourishing yin and nourishing stomach, clearing heat and dispelling dampness and so on. It has developed a new way of thinking for the clinical treatment of CAG in traditional Chinese medicine. 

/pdf/analysis-of-medication-law-in-treatment-of-chronic-atrophic-1shaqsff.pdf

Analysis of Medication Law in Treatment of Chronic Atrophic Gastritis Based on TCM Inheritance Auxiliary System

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An effector of 'Candidatus Liberibacter asiaticus' manipulates autophagy to promote bacterial infection.

Curcumol alleviates liver fibrosis through inducing autophagy and ferroptosis in hepatic stellate cells

Analysis of Medication Law in Treatment of Chronic Atrophic Gastritis Based on TCM Inheritance Auxiliary System