Tissue & cell · 2026
Claudin-2 overexpression protects against methamphetamine-induced apoptosis in renal tubular cells.
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Lu Shuang, Yan Weitao, Wang Lewen, Zhao Dongsheng, Hu Guoqian, Xiong Kun, Tang Jin
Аннотация
BACKGROUND: Methamphetamine (METH) is a synthetic, non-catecholamine sympathomimetic drug that is highly susceptible to drug dependence. Abuse of this drug can cause immense damage to the body and even lead to death. Long-term abuse of METH will lead to renal failure, but its specific pathological mechanism is still unclear.
METHODS: We established a mouse model of METH poisoning and evaluated renal function through HE staining, serum creatinine (Cr), and urea nitrogen (BUN) levels, whiles also assessing claudin-2 and cleaved caspase-3 expression. We analysed the changes of claudin-2 expression and apoptosis in HK-2 cells under different concentration of METH. Moreover, we examined the effects of claudin-2 overexpression on METH-induced apoptosis used by Flow cytometry and Western blot analyses in vitro.
RESULTS: METH caused cells to shrink, and serum creatinine and urea nitrogen levels were also significantly higher than those in the sham group. In vivo, METH treatment increased the expression of cleaved caspase-3 and decreased the expression of claudin-2 in kidney of mice. In vitro, METH treatment caused apoptosis in a concentration dependent manner and decreased the expression of claudin-2. Overexpression of claudin-2 could attenuate METH-induced HK-2 cell apoptosis.
CONCLUSION: These results suggest that claudin-2 plays crucial roles in METH-induced apoptosis and may be a new potential target in METH-induced renal injury.
METHODS: We established a mouse model of METH poisoning and evaluated renal function through HE staining, serum creatinine (Cr), and urea nitrogen (BUN) levels, whiles also assessing claudin-2 and cleaved caspase-3 expression. We analysed the changes of claudin-2 expression and apoptosis in HK-2 cells under different concentration of METH. Moreover, we examined the effects of claudin-2 overexpression on METH-induced apoptosis used by Flow cytometry and Western blot analyses in vitro.
RESULTS: METH caused cells to shrink, and serum creatinine and urea nitrogen levels were also significantly higher than those in the sham group. In vivo, METH treatment increased the expression of cleaved caspase-3 and decreased the expression of claudin-2 in kidney of mice. In vitro, METH treatment caused apoptosis in a concentration dependent manner and decreased the expression of claudin-2. Overexpression of claudin-2 could attenuate METH-induced HK-2 cell apoptosis.
CONCLUSION: These results suggest that claudin-2 plays crucial roles in METH-induced apoptosis and may be a new potential target in METH-induced renal injury.