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PIP is well known antioxidant that showed neuroprotection against cerebral ischemia (2h) /reperfusion (24h) (I/R) injury. However, it can degrade very easily in presence of UV-R/sunlight. Here, comparative study of non-irradiated and UV-B (0.6mW/cm2) irradiated PIP was performed against cerebral I/R injury. First, the dose dependence evaluation of neuroscore was investigated after the non-irradiated PIP intravenously (2.5, 5, 10 mg/kg b w, i.v.) treatment. The neuroprotective outcome of UV-B irradiated and non-irradiated PIP (5 mg/kg b w, i.v.) against cerebral I/R in SD rats was investigated through evaluation of neuroscore and quantification of infarct volume by TTC staining. The result of photodegradation of PIP under UV-B irradiation revealed the formation of photoproducts. There were no changes in Cortical and mitochondrial ROS level and antioxidant defence enzyme (CuZn-SOD, Mn-SOD, and catalase) and non-enzyme (LPO, protein carbonyl and reduced glutathione) activities in UV-B irradiated compare vehicle group. Thus, our results demonstrated that PIP could lose its parent structure in presence of UV-B and attenuates its neuroprotective efficacy. Thus, UV-B exposure must be avoided during dietary intake of PIP to obtain best neuroprotective response.

PIP is well known antioxidant that showed neuroprotection against cerebral ischemia (2h) /reperfusion (24h) (I/R) injury. However, it can degrade very easily in presence of UV-R/sunlight. Here, comparative study of non-irradiated and UV-B (0.6mW/cm2) irradiated PIP was performed against cerebral I/R injury. First, the dose dependence evaluation of neuroscore was investigated after the non-irradiated PIP intravenously (2.5, 5, 10 mg/kg b w, i.v.) treatment. The neuroprotective outcome of UV-B irradiated and non-irradiated PIP (5 mg/kg b w, i.v.) against cerebral I/R in SD rats was investigated through evaluation of neuroscore and quantification of infarct volume by TTC staining. The result of photodegradation of PIP under UV-B irradiation revealed the formation of photoproducts. There were no changes in Cortical and mitochondrial ROS level and antioxidant defence enzyme (CuZn-SOD, Mn-SOD, and catalase) and non-enzyme (LPO, protein carbonyl and reduced glutathione) activities in UV-B irradiated compare vehicle group. Thus, our results demonstrated that PIP could lose its parent structure in presence of UV-B and attenuates its neuroprotective efficacy. Thus, UV-B exposure must be avoided during dietary intake of PIP to obtain best neuroprotective response.

PIP is well known antioxidant that showed neuroprotection against cerebral ischemia (2h) /reperfusion (24h) (I/R) injury. However, it can degrade very easily in presence of UV-R/sunlight. Here, comparative study of non-irradiated and UV-B (0.6mW/cm2) irradiated PIP was performed against cerebral I/R injury. First, the dose dependence evaluation of neuroscore was investigated after the non-irradiated PIP intravenously (2.5, 5, 10 mg/kg b w, i.v.) treatment. The neuroprotective outcome of UV-B irradiated and non-irradiated PIP (5 mg/kg b w, i.v.) against cerebral I/R in SD rats was investigated through evaluation of neuroscore and quantification of infarct volume by TTC staining. The result of photodegradation of PIP under UV-B irradiation revealed the formation of photoproducts. There were no changes in Cortical and mitochondrial ROS level and antioxidant defence enzyme (CuZn-SOD, Mn-SOD, and catalase) and non-enzyme (LPO, protein carbonyl and reduced glutathione) activities in UV-B irradiated compare vehicle group. Thus, our results demonstrated that PIP could lose its parent structure in presence of UV-B and attenuates its neuroprotective efficacy. Thus, UV-B exposure must be avoided during dietary intake of PIP to obtain best neuroprotective response.