RESUMEN
Reflux esophagitis is an inflammatory disease of esophageal mucosa damage caused by the reflux of gastric contents into the esophagus. Its incidence is on the rise， and it has become an important precancerous disease of esophageal cancer. Studies have shown that the continuous inflammatory response stimulates the esophageal mucosa， causing abnormal proliferation of esophageal epithelial cells and damage to esophageal mucosal tissue， which eventually leads to the occurrence of heterogeneous hyperplasia and even carcinogenesis. The nuclear transcription factor-kappa B （NF-κB） signaling pathway is one of the most classical inflammatory and cancer signaling pathways. It has been found that abnormal activation of the NF-κB signaling pathway is crucial to the development and prognosis of reflux esophagitis and esophageal cancer. It is widely involved in the proliferation， autophagy， apoptosis， and inflammatory response of esophageal epithelial cells and tumor cells， accelerating the transformation of reflux esophagitis to esophageal cancer and making it a potential target for the treatment of reflux esophagitis and esophageal cancer. Currently， there is no specific treatment for reflux esophagitis and esophageal cancer， and large side effects often appear. Therefore， finding a promising and safe drug remains a top priority. In recent years， traditional Chinese medicine scholars have conducted a lot of research on NF-κB signaling pathway， and the results indicate that NF-κB signaling pathway is an important potential target for traditional Chinese medicine to prevent and treat reflux esophagitis and esophageal cancer， but there is a lack of comprehensive and systematic elaboration. Therefore， this paper summarized the relevant studies in recent years， analyzed the relationship among NF-κB signaling pathway， reflux esophagitis， esophageal cancer， and transformation from inflammation to cancer， and reviewed the research literature on the regulation of the NF-κB signaling pathway in traditional Chinese medicine to prevent and treat reflux esophagitis and esophageal cancer， so as to provide new ideas for the prevention and treatment of reflux esophagitis and esophageal cancer.
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Esophageal cancer （EC） is a common malignant tumor of the digestive system with an extremely poor prognosis. MicroRNA （miRNA） is an important regulator in tumor occurrence and development， and can participate in malignant biological behaviors such as tumor cell proliferation， invasion， metastasis and apoptosis. Traditional Chinese medicine has the characteristics of accurate curative effects， wide range of effects， and few side effects. The review uses miRNA as the entry point to systematically elaborate on the mechanism of traditional Chinese medicine-mediated miRNA intervening in EC. The results showed that active ingredients of traditional Chinese medicine （including curcumin， Tussilago farfara polysaccharides， Atractylodes macrocephala polysaccharides and ophiopogonin B） and Dougen guanshitong oral liquid could up-regulate the expressions of miRNAs such as miRNA-532-3p （miR-532-3p）， miR-551b-3p， miR-99a， miR-34a， miR-199a-3p and miR-377； and the active ingredients/parts of traditional Chinese medicine （including chrysin and Actinidia arguta extract）， and Chinese herbal formulas （including Chaihu shugan san combined with Xuanfu daizhe decoction and Modified jupi zhuru decoction） could down-regulate the expressions of miRNAs such as miR-199a-3p， miR-451 and miR-21， which could regulate the expressions of signaling pathways （phosphoinositide 3-kinase/protein kinase B， etc.） or their downstream protein（zinc-finger and homeobox protein 1， etc.） or enzymes（thymidine kinase-1， etc.）， inhibit the proliferation， invasion and metastasis of EC cells and induce apoptosis， thereby ultimately achieving the purpose of preventing the disease from aggravating.
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Pancreatic cancer is one of the most destructive malignant tumors； the pathogenesis of this disease is complex and is closely related to genetic susceptibility， chronic pancreatitis， and gene mutations in signaling pathways. The phosphoinositide 3- kinase （PI3K）/protein kinase B （Akt） signaling pathway is a classical cancer signaling pathway that is aberrantly activated in pancreatic cancer cells. In recent years， it has been found that traditional Chinese medicine （TCM） monomers show special activity in the treatment of pancreatic cancer and can be potential drug for the treatment of pancreatic cancer. Based on PI3K/Akt signaling pathway， this paper summarizes the mechanism of TCM monomer intervening in pancreatic cancer and finds that TCM monomer of alkaloids （sinomenine， dictamnine， dauricine， etc.）， terpenoids （saikosaponin A， linderalactone， isoalantolactone， etc.）， phenols （6-gingerol， curcumin， pterostilbene， etc.）， flavonoids （fisetin， kaempferol， quercetin， etc.） and quinones （β-hydroxyisovaleryl shikonin， rhein， lucidone， etc.） can inhibit the proliferation， invasion and migration of pancreatic cancer cells， regulate autophagy and apoptosis， and then inhibit the pathological process of pancreatic cancer by inhibiting PI3K/Akt signaling pathway.
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Colorectal cancer （CRC） is one of the leading causes of cancer-related deaths worldwide， with increasing incidence and mortality rates. The disease often develops covertly and lacks specific symptoms in its early stages， leading to late-stage diagnoses in most patients. It has become a prominent research topic in the field of digestive system tumors. The exact mechanisms underlying CRC are not yet clear and involve factors such as genetics， gene mutations， inflammatory responses， and aberrant activation of tumor-related signaling pathways. Nuclear factor-kappa B （NF-κB） is a crucial transcription factor that participates in various biological processes， including inflammatory responses， immune responses， cell proliferation， and apoptosis. Research suggests that NF-κB， serving as a molecular link between inflammation and cancer， is highly expressed in CRC. It promotes the occurrence and development of CRC by regulating the activity of target genes such as cell pro-inflammatory factors， chemokines， angiogenic factors， metastasis factors， and anti-apoptotic proteins. Currently， common treatments for CRC include surgery， radiation therapy， and chemotherapy drugs like 5-fluorouracil. However， these treatments have limitations such as significant adverse reactions， high metastasis rates， and the development of drug resistance. Therefore， the search for effective， low-adverse-reaction drugs to replace or supplement current treatments is essential. In recent years， traditional Chinese medicine （TCM） has shown some effectiveness in preventing and treating CRC. TCM has been found to inhibit the growth of CRC cells by modulating the NF-κB signaling pathway， playing a positive role in the occurrence and progression of CRC. Based on the asthenia in origin and sthenia in superficiality and deficiency-excess in complexity in CRC， this article summarized and analyzed the mechanisms and effects of TCM interventions targeting the NF-κB signaling pathway in CRC， and reviewed advances of 10 Chinese medicinal compound formulas and 37 Chinese medicinal monomer components of different types， including flavonoids， phenols， alkaloids， glycosides， and terpenoids with the effects of dispelling pathogenic factors， reinforcing healthy qi， and removing toxins in the prevention and treatment of CRC by targeting the NF-κB pathway. It is found that Chinese medicine can inhibit CRC cell proliferation， invasion， metastasis， angiogenesis， and inflammation by modulating the NF-κB signaling pathway， induce cell apoptosis， restore drug and radiation sensitivity， and counteract CRC. This article is expected to provide insights and references for the in-depth exploration and treatment of CRC mechanisms.
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Colorectal cancer （CRC）， a malignant tumor of the digestive system， originates from the colorectal mucosa epithelium and is usually asymptomatic until it progresses to an advanced stage. With high incidence around the globe and the increasingly younger patients， this disease poses a serious threat to the health and lives of the patients. Although the pathogenesis of this disease is not fully understood， it is generally believed that it is associated with autophagy， apoptosis， and inflammation. Autophagy and apoptosis as two types of programmed cell death are subject to complex interactive regulation， and the imbalance between them is closely related to the occurrence， development， and prognosis of a variety of diseases. Studies have shown that autophagy-apoptosis balance plays a key role in CRC. On the one hand， autophagy and apoptosis coordinate with each other to inhibit CRC cell growth. On the other hand， autophagy can antagonize apoptosis to promote CRC cell growth. In clinical practice， surgery is often combined with radiotherapy and chemotherapy to treat CRC， which can control the progression of CRC to a certain extent but has serious adverse effects and poor long-term results. In recent years， traditional Chinese medicine （TCM） has been proved to be effective in the treatment of CRC. Studies have shown that numerous herbal active components can promote CRC cell death by regulating the autophagy-apoptosis balance， thereby blocking the progression of this disease. The process of autophagy-apoptosis balance in regulating cell activities has similar theoretical connotations with the Yin and Yang theory of TCM. Applying TCM in regulating autophagy-apoptosis balance at various stages of CRC has become a frontier， while the comprehensive elaboration remains to be conducted. By reviewing the relevant studies in recent years， this paper introduces the correlation between the Yin and Yang theory and the autophagy-apoptosis balance， the role of autophagy-apoptosis balance in CRC， and the research progress in the application of 27 Chinese herbal active components such as flavonoids， terpenoids， glycosides， and phenols capable of regulating autophagy-apoptosis balance in the treatment of CRC. The active components in Chinese medicines can recover the autophagy-apoptosis balance in CRC by acting on microtuble-associated protein 1 light chain 3（LC3）， Beclin-1， and B-cell lymphoma-2（Bcl-2）to regulate multiple signaling pathways such as protein kinase B（Akt）/mammalian target of rapamycin（mTOR）and reavtive oxygen species（ROS）/ c-Jun N-terminal kinase（JNK）， thus balancing Yin and Yang. This review aims to provide a reference for the treatment of CRC and the development of new drugs.
RESUMEN
Objective To investigate the effects of the c-Jun N-terminal kinase (JNK)pathway on isoflurane induced neuronal apoptosis and the proteins expression of phospho-JNK,Bcl-2 and Bax in the hippocampi of neonatal rats.Methods Forty-eight neonatal rats at postnatal day 7 (P7) were randomly assigned into 4 groups:DMSO control group (group D),SP600125 control group (group SP30),isoflurane + DMSO group (group Iso +D),isoflurane + SP600125 group (group Iso + SP30).Rats were exposed to air (control group) or 1.1％ isoflurane (isoflurane group) for 4 h.The JNK inhibitor SP600125 at 30 μg or 12％ DMSO 5 μl was intraventricularly administered 20 min before the exposure.The brains of some rats in each group were perfused and embedded by paraffin 6 h after the exposure.Neuronal apoptosis in the hippocampi CA1 area was detected by TUNEL (n =6).The fresh hippocampi of other rats in each group were dissected 6 h after the exposure and the proteins expression of phospho-JNK,Bcl-2 and Bax were detected by Western blot (n =6).One way ANOVA were used for data analysis among groups.Results The number of TUNEL positive cells in the hippocampal CA1 regions in group Iso +D (135.72 ±21.26 per mm2) increased by 5 folds compared with group D (24.07 ± 1.35 per mm2) (P＜0.01) ;while the number of apoptotic cells in group Iso + SP30 (42.49 ± 5.56 per mm2) decreased by 84％ (P ＜ 0.05)compared with group Iso + D.The expression of phospho-JNK p46 kd in group Iso + D increased by 44.1％ (P ＜0.01),while both phospho-JNK at p46kd and at p54kd in group Iso + SP30 decreased significantly (P＜0.05,P ＜0.01) compared with group Iso + D.The protein expression of Bax increased 1.5 folds (P＜0.05) and Bcl-2 decreased by 42.2％ (P＜0.05) in group Iso + D compared to group D;while SP600125 significantly decreased expression of Bax (P ＜0.05) and increased expression of Bcl-2 (P＜0.01).Conclusion JNK activation contributes to isoflurane-induced neuroapoptosis in the developing brain.Maintaining Bcl-2 expression and inhibiting Bax expression may be involved in the neuroprotective effects of SP600125.