The effect of cordycepin on brain oxidative stress and protein expression in streptozotocin-induced diabetic mice

Diabetes mellitus (DM) is characterized by metabolic disorders and psychological deficits, including cognitive decline. Here, we investigated the effect of cordycepin on oxidative stress and protein expression in the brains of diabetic mice. Twenty-four mice were divided into four groups, one comprising untreated healthy mice (N); one comprising healthy mice treated with cordycepin (24 mg/kg body weight) (N+Cor); one comprising untreated DM mice; and one comprising DM mice treated with cordycepin (24 mg/kg body weight) (DM+Cor). After 14 days of treatment, cognitive behavior was assessed using the novel object recognition (NOR) test. The brain levels of oxidative stress markers (glutathione, catalase, and superoxide dismutase) were examined using the respective detection kits. Protein expression in brain tissues was assessed by liquid chromatography with tandem mass spectrometry (LC–MS/MS); the functions of the identified proteins were annotated by PANTHER, while major protein–protein interactions were assessed using STITCH. We found that cordycepin treatment significantly decreased body weight and food and water intake in the DM+Cor group compared with that in the DM group; however, no differences in blood glucose levels were found between the two groups. Cordycepin treatment significantly reversed cognitive decline in diabetic mice in the NOR test and ameliorated antioxidant defenses. Additionally, we identified ULK1 isoform 2, a protein associated with cognitive function via the activated AMPK and autophagic pathways, as being uniquely expressed in the DM+Cor group. Our findings provide novel insights into the cellular mechanisms underlying how cordycepin improves cognitive decline in diabetic mice.     

Natural infection of leptospirosis and melioidosis in long-tailed macaques (Macaca fascicularis) in Thailand

This study aimed to determine the incidence of leptospirosis and melioidosis in long-tailed macaques (Macaca fascicularis) in Thailand. Serum samples from 223 monkeys were subjected to the Lepto Latex Test and indirect hemagglutination (IHA) test to detect antibodies against Leptospira spp. and Burkholderia pseudomallei. The microagglutination test (MAT) was used to identify serovars of Leptospira spp. Conventional PCR for the LipL32 gene of L. interogans and the BPSS0120 and btfc-orf18 genes of B. pseudomallei was used for molecular detection. The overall seroprevalence of leptospirosis and melioidosis was 2.69% (95% confidence interval (CI): 0.99–5.76%) and 14.35% (95% CI: 10.03–19.65%), respectively. Six samples that showed positive MAT results were also positive for IHA. The serovars of Leptospira were Ranarum (5/6), Shermani (6/6), and both (5/6). Conventional PCR for the LipL32 gene of Leptospira spp. was positive in 10.31% of the samples (95% CI: 5.56–13.51%). However, there were no positive results for BPSS0120 and btfc-orf18 in B. pseudomallei. Active infection was detected only for leptospirosis; however, it can be assumed that pathogen exposure occurred in this group of animals because immunity could be detected. The routes of infection and elimination pathways of both bacteria remain unclear, and the mechanism of protection in non-human primates needs to be elucidated in further studies. Moreover, this health issue should be considered to prevent human infections in monkeys and their environment.