Stability of population genetic structure in large yellow croaker (Larimichthys crocea): Insights from temporal, geographical factors, and artificial restocking processes.

Despite concerns about overfishing and the potential impact of release programs on wild populations, our study of 3116 individuals from 13 wild populations and 2787 individuals from two cultured populations in Zhejiang and Fujian provinces spanning 2008 to 2023 reveals a relatively stable genetic diversity in Larimichthys crocea. Surprisingly, the genetic diversity of wild large yellow croaker populations has remained consistent over the years, suggesting minimal influence from population declines due to overfishing. With the exception of populations in Sansha Bay and Luoyuan Bay, no significant genetic differences were observed among wild populations, indicating a single panmictic genetic population across the East and South China seas. Notably, significant genetic differentiation exists between cultured and wild populations, suggesting a possible limited genetic adaptation of cultured-released individuals to the wild environment. The genetic differences observed between the Sansha Bay, with its adjacent Luoyuan Bay populations, and other wild populations underscore the dual effects of habitat environment and farming activities on the genetic structure of large yellow croaker. Our findings suggest that, despite declines in population numbers due to overfishing and expands extensive cultured releases, the genetic diversity of L. crocea populations remains largely unaffected. Moreover, the L. crocea population along the Chinese coast appears to form a single panmictic population with considerable genetic diversity.

Angiotensin II receptor type 1 blocker candesartan improves morphine tolerance by reducing morphine­induced inflammatory response and cellular activation of BV2 cells via the PPARγ/AMPK signaling pathway.

Morphine is the most common drug of choice in clinical pain management; however, morphine tolerance presents a significant clinical challenge. The pathogenesis of morphine tolerance is known to be closely associated with angiotensin II receptor type 1 (AT1R) in microglia. As an AT1R antagonist, candesartan may serve an important role in regulating morphine tolerance. Therefore, the present study aimed to investigate the role of candesartan in morphine tolerance, and to explore the underlying mechanism. To meet this aim, BV2 microglial cells were treated with morphine or candesartan alone, or as a combination, and the expression levels of AT1R in BV2 cells were detected by reverse transcription­quantitative PCR (RT­qPCR) and western blotting. The levels of the inflammatory cytokines tumor necrosis factor­α, interleukin (IL)­1ß and IL­6 were subsequently detected by ELISA and western blotting. In addition, immunofluorescence analysis, western blotting and RT­qPCR were used to detect the expression levels of the BV2 cell activation marker, ionized calcium­binding adaptor molecule 1 (IBA­1). Western blotting was also used to detect the expression levels of peroxisome proliferator­activated receptor­Î³/AMP­activated protein kinase (PPARγ/AMPK) signaling pathway­associated proteins. Finally, the cells were treated with the PPARγ antagonist GW9662 and the AMPK inhibitor compound C to further explore the mechanism underlying the effects of candesartan on improving morphine tolerance. The expression levels of AT1R were revealed to be significantly increased following morphine induction; however, candesartan treatment inhibited the expression levels of AT1R, the levels of inflammatory cytokines and the protein expression levels of IBA­1 in morphine­induced BV2 cells in a dose­dependent manner. These processes may be associated with activation of the PPARγ/AMPK signaling pathway. Taken together, the present study revealed that treatment with candesartan reduced morphine­induced inflammatory response and cellular activation of BV2 cells via PPARγ/AMPK signaling.