Epilepsy is a heterogeneous disease with a very complex etiological mechanism, characterized by recurrent and unpredictable abnormal neuronal discharge. Epilepsy patients mainly rely on oral antiseizure medication (ASMs) the for treatment and control of disease progression. However, about 30% patients are resistance to ASMs, leading to the inability to alleviate and cure seizures, which gradually evolve into refractory epilepsy. The most common type of intractable epilepsy is temporal lobe epilepsy. Therefore, in-depth exploration of the causes and molecular mechanisms of seizures is the key to find new methods for treating refractory epilepsy. Mitochondria are important organelles within cells, providing abundant energy to neurons and continuously driving their activity. Neurons rely on mitochondria for complex neurotransmitter transmission, synaptic plasticity processes, and the establishment of membrane excitability. The process by which the autophagy system degrades and metabolizes damaged mitochondria through lysosomes is called mitophagy. Mitophagy is a specific autophagic pathway that maintains cellular structure and function. Mitochondrial dysfunction can produce harmful reactive oxygen species, damage cell proteins and DNA, or trigger programmed cell death. Mitophagy helps maintain mitochondrial quality control and quantity regulation in various cell types, and is closely related to the occurrence and development of epilepsy. The imbalance of mitophagy regulation is one of the causes of abnormal neuronal discharge and epileptic seizures. Understanding its related mechanisms is crucial for the treatment and control of the progression of epilepsy in patients.
Objective To establish perineural invasion xenograft model of hilar cholangiocarcinoma. Methods The cultured cells of cholangiocarcinoma cell line QBC939 were inoculated subcutaneously in the nude mice so as toestablish primary subcutaneous model of cholangiocarcinoma. The primary tumor tissues were inoculated intraperitoneallyaround the liver in the nude mice so as to establish the second generation intraperitoneal xenograft model. The successful xenografted tumor tissues were obtained for anatomical and pathological examinations. Results The tumor formation rate of primary subcutaneous xenograft of hilar cholangiocarcinoma was 100% （5/5）， and no nerve infiltration was observed. The tumor formation rate of the second generation intraperitoneal xenograft was 45% （9/20）， and two mice （2/9， 22%） manifested nerve infiltration. The rate of nerve infiltration was 10% （2/20）， and the tumor cells had different size and diversity， irregular shape， low differentiation， decreased cytoplasm and nucleus karyomegaly， visible atypical and fission phase， and no obvious gland tube structure by pathological examination. Conclusions Hilar cholangiocarcinoma cell has the particular features of perineural invasion， it is a good experiment platform for researching the mode and biological characteristics of perineural invasion of hilar cholangiocarcinoma by applicated QBC939 cell lines to establish the perineural invasion xenograft model of cholangiocarcinoma.