ABSTRACT
Objective To investigate the level of deltamethrin resistance and mutation sites in the sodium iron channel gene in Rhipicephalus microplus in Huaihua City, Hunan Province, and to examine the correlation between deltamethrin resistance and mutation sites in the sodium iron channel gene in Rh. microplus. Methods Rh. microplus was sampled from multiple yellow cattle farms in Huaihua City, Hunan Province from June to September 2022, and the level of resistance to deltamethrin was determined in ticks using the adult immersion test. The sodium iron channel domain III gene was amplified in deltamethrin-resistant and wild-type Rh. microplus using PCR assay. Following sequencing and sequence alignment, mutation sites were detected in bases. The sodium iron channel domain III gene in Rh. microplus was translated, and the signal peptide, transmembrane domain, and phosphorylation and glycosylation sites were detected in amino acid sequences. The tertiary structures of the sodium iron channel domain III protein of deltamethrin-resistant and wild-type Rh. microplus were deduced and compared, and the association be tween mutation sites in bases and resistance to deltamethrin was examined in Rh. microplus according the level of deltamethrin resistance, sequence alignment and protein tertiary structure. Results The median (LC50) and 95% lethal concentrations (LC95) of deltamethrin were 121.39 mg/L and 952.61 mg/L against Rh. microplus, with a resistance factor of 9.24 and level II resistance. The sequence of the sodium ion channel domain III gene was 1 010 bp in size, and mutation sites were detected in two neighboring bases in the sequence of the sodium ion channel domain III gene in deltamethrin-resistant Rh. microplus. Although no signal peptides were found in the sodium iron channel domain III protein of deltamethrin-resistant or wild-type Rh. microplus, 6 trans-membrane domains, 42 phosphorylation sites and 8 glycosylation sites were identified, with a significant difference in the tertiary structure of the sodium iron channel domain III protein between deltamethrin-resistant and wild-type Rh. microplus. Conclusions Level II resistance to deltamethrin is detected in Rh. microplus in Huaihua City, Hunan Province, and two mutation sites that correlate with the emergence of deltamethrin resistance are identified in the sequence of the sodium iron channel domain III gene in deltamethrin-resistant Rh. microplus.
ABSTRACT
AIM:To establish a mouse model of immuno-inflammation in central nervous system (CNS) associated with cognitive dysfunction.METHODS:C57BL/6J male mice were divided into 3 groups.Lipopolysaccharide (LPS) was intraperitoneally injected into the mice to induce cognitive impairment.Morris water maze test, passive avoidance test and pole test were used to observe the behavioral changes of mice.The histomorphology was analyzed by the method of immunofluorescence.The detailed molecular mechanism was determined by Western blot.RESULTS:Compared with saline group, LPS induced mouse sickness behavior and memory loss.Microglia activation and neuronal loss in the hippocampus were observed.The expression of neuroinflammatory proteins COX-2 and iNOS in the brain of LPS-induced mice was increased.CONCLUSION:Intraperitoneal injection of LPS induces cognitive dysfunction in mice.
ABSTRACT
AIM:To investigate the protective effect of lycopene on primary mouse cerebrocortical neurons ex -posed to tert-butyl hydroperoxide ( t-BHP) and its mechanisms of in vitro.METHODS:Primary cerebrocortical neurons of newborn C57 mice were extracted and divided into normal group , t-BHP group, lycopene +t-BHP group and lycopene group.The neuronal damage was induced by t-BHP exposure for 24 h, and the cell viability was examined by MTT assay . ROS content was measured by flow cytometry , and the protein levels of Bax , Bcl-2, caspase-3, cleaved caspase-3 and cyto-chrome C were examined by Western blot .RESULTS:The primary mouse cortical neurons expressed MAP-2 protein.Ly-copene at concentration of 4μmol/L reversed the decrease in cell viability .Flow cytometry revealed that lycopene treatment attenuated ROS content under the condition of t-BHP exposure.In addition, the protein level of Bcl-2 was increased, and the expression of Bax , cleaved caspase-3 and cytochrome-C was suppressed in lycopene +t-BHP group.CONCLUSION:The protective effect of lycopene on cortical neurons with t-BHP-induced injury may be involved in the mechanism of neuro-nal antioxidative response by down-regulating caspase-3 and Bax/Bcl-2 through the mitochondrial apoptotic pathway .